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InГ©s Sastre Video

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Welcome and thank you very much for participating in this Congress. This is the first time that a joint FrancoArgentine Immunology meeting has been organized.

France and Argentina are two countries with major interest in basic and applied immunology. We hope that this congress will reinforce scientific exchange and initiate new solid and long-lasting collaborations in immunology between the 2 countries so as to increase international visibility of the FrancoArgentine Immunology Network: 14 at the academic level: several collaborations have already been initiated and we hope that several others will be inspired by these three days of meetings.

We hope that everybody will appreciate this meeting in Buenos Aires and we hope that this event will be the first of a long series of fruitful scientific exchanges between the two countries.

Wellcoming words E. Since then we have continuously worked in order to reach other groups using this methodology for diagnosis or research.

On this occasion, by means of the Pre-Conference Course of the SAI, our objective is to present an update on methodology and analysis software through an outstanding group of speakers from Argentina and abroad.

It is our wish that all the topics dealt with in this event will help enhance your learning experience and background in the immunology field.

We have used 2-photon dynamic imaging to analyze T cells and DCs in intact lymph nodes and tumors ex vivo or intravitally. We showed that stable T cell-DC interactions correlate with the induction of effective immunity, while the induction of tolerance involves brief, unstable contacts.

The adhesion molecule ICAM-1 plays a central role in this process. We also analyzed the modes of tumor invasion by cytotoxic T cells, and, more recently, the mechanisms of inhibition of anti tumor immune responses by regulatory T cells.

Together these results showed that the control of the dynamics of T cell-DC interactions plays a critical role in the outcome of T cell-mediated immune responses.

Monoclonal antibodies to CD3 promote immune tolerance. This strategy has been the matter of extensive experimental studies in models of autoimmunity such as autoimmune insulin-dependent diabetes.

Data from our laboratory were the first to show that in non obese diabetic NOD mice CD3-specific antibodies could reverse recent onset disease by restoring tolerance to beta-cell antigens.

Thus, in NOD mice presenting full-blown diabetes, a five consecutive day treatment with low doses of CD3-specific antibody induced complete and durable disease remission in absence of insulin treatment.

Recently, these results were successfully transferred to the clinic in patients presenting new onset autoimmune diabetes. The present challenge is first, to build on these results to set the use of CD3-specific monoclonal antibodies as an established therapy in well-selected subsets of patients presenting with established autoimmunity and second, to extend their use to the organ transplantation field, where they were first introduced, taking benefit of their unique tolerance-promoting capacities.

Results will be discussed in the context of autoimmune diseases in which antibodies play a pathognomonic role. Breakdown of self-tolerance: Autoimmune Orchitis 16 Vanesa A.

Facultad de Medicina. Universidad de Buenos Aires. Spermatogenesis represents challenges to the immune system, as male gametes appear long after the establishment of immune tolerance mechanisms.

Disruption of the immune privileged status of the testis following trauma, tumor, or autoimmune orchitis often results in male infertility.

DC maturation state is a control point for the induction of peripheral tolerance or autoimmunity.

Investigation of EAO will help to understand the intricate interplay among tolerance mechanisms and autoimmunity. Animal models of CNS autoimmunity: what have we learned?

The cause of MS is still mostly unknown. Demyelination in the central nervous system in MS is thought to be mainly mediated by T helper 1 cells, although this dogma is currently heavily re discussed since recent evidence suggests an active pathogenic role of CD8 T cells in MS, which recapitulates earlier suggestions that virus may have pathogenic role in MS.

Currently the unraveling of immune-mediated pathogenesis in MS relies mostly on animal models. So far there is not one animal model that reflects all aspects seen in MS, but still the many different models are very suitable for targeting specific aspects of this disease.

By using rodent models we pinpointed several cellular and molecular pathways of potential relevance for human inflammatory diseases of the central nervous system.

The lessons learned from these models will be discussed. The full extent of differences and similarities between iTreg and nTreg cells is the subject of this presentation.

We speculate that iTreg cell development is driven by the need to maintain a non-inflammatory environment in the gut, to suppress immune responses to environmental and food allergens, and to decrease chronic inflammation, whereas nTreg cells prevent autoimmunity and raise the activation threshold for all immune responses.

Rosenzweig 17 Infectious Diseases Susceptibility Unit. However, a small number of patients develop serious, life-threatening hepatitis.

To understand reasons for this great variability in disease severity, we examined 30 Argentinean patients with HAV-induced acute liver failure in a case-controlled, cross-sectional, observational study.

In addition, we propose a pathophysiological molecular mechanism by which NKT cells mediate the liver injury that develops with HAV infection, a mechanism that may be related to one that protects against asthma and allergy.

We report a new molecular mechanism of disease in patients with Xlinked EDA-ID caused by mutations that affect the poly-ubiquitin binding of NEMO rather than its production and folding.

We found a novel mutation in exon 3 of TNFRSF6, in two patients from a consanguineous family, presented in homozygous state.

This mutation changes a cytosine for a tyrosine C91Y in one of the conservative domain of the extracellular region, cysteine rich domain 2 CRD2.

Interestingly, this particular change was found in three other patients from three unrelated families, in heterozygous state. All these SNPs are highly polymorphic and we found the ancestral allele in all of them except for c.

These data strongly suggest that the C91Y mutated allele originated from a single founder. We applied a modified likelihood-based method to estimate the age of the most recent common ancestor carrying mutation C91Y.

Extent of haplotype sharing and variability of microsatellite alleles in C91Y chromosomes suggest that this mutation arose approximately years ago.

Taking into account that GTATCC haplotype was not found in our control group nor in a previous report on Caucausian subjects from USA, we have undertaken a large study on Native American Argentinean populations, to test if the unique haplotype carrying this novel mutation is restricted to a particular ethnic group.

For instance, the SNP c. Invasive pneumococcal disease leads to significant morbidity and mortality all over the world. Immunization with pneumococcal polysaccharide 23 valent vaccine is useful to evaluate antibody response to polysaccharide antigen in children over 2 years of age.

At present we evaluate polysaccharide response by measuring antiboby against 10 pneumoccocal specific serotypes 1, 3, 5, 6B, 7F, 9V, 14, 18C, 19F, 23F.

Pneumococcal conjugate vaccine with protein carrier, has been useful to protect children younger than 2 years of age. Given the massive use of 7 valent conjugate vaccine, which produces a humoral immune response different from PLS vaccine, it is difficult to assess specific polysaccharide response in children who have received both vaccines.

The aim of this study is to evaluate the usefulness of an extended panel of 12 specific serotypes, 6 of which are present in polysaccharide vaccine 1, 3, 5, 7F, 11A y 33F and the other 6 are present in both vaccines 6B, 9V, 14, 18C, 19F, 23F , in children older than 2 years, who have received 23 valent and 7 valent conjugate pneumococcal vaccines.

Buenos Aires. Argentina; 3Dept. Melanoma and severe opportunistic infections, mainly fungal infections, are rare in healthy pediatric individuals.

Here, we present a case of a 13 year old male, second son from non-consanguineous parents with clinical background of atopy and upper airway infections.

At the age of 12, the patient presented a melanoma in the right 19 ear, which was successfully treated by surgery.

One year later he developed a lobar pneumonia due to Cryptococcus neoformans detected in a lung biopsy, accompanied by stools with blood.

Thus, the patient was subjected to additional immunological studies, which ruled out the occurrence of classical cellular and humoral primary and secondary immunodeficiencies.

Thus, the NK cell compartment was further investigated, assuming that an impaired NK cell function could lead to a weakened immune surveillance and the development of the observed clinical symptoms.

NK cells of this patient, although normal in number, contain an unexpectedly high percentage of CD56bright cells Classically they are characterized by susceptibility to infections.

However, autoimmune manifestations, essentially autoimmune cytopenias anemia, thrombocytopenia and neutropenia , can also be observed in PIDs as a consequence of either defective central selection or defective peripheral self-tolerance.

Defect of peripheral tolerance can be observed in the context of impaired natural Tregs nTregs development or functions.

Recently, we described three patients presenting with a severe IPEX-like syndrome starting in childhood and susceptibility to severe CMV infections.

We identified inherited mutations of the IL2Ra gene. Activated T cells were devoid of CD25 expression. Finally, we also observed a complete nTregs deficiency in patients presenting with a profound calcium influx deficiency leading to a paradoxical presentation of severe combined immunodeficiency and autoimmune manifestations.

Altogether these observations highlight the central role of nTregs in the maintenance of self-tolerance and may provide mechanistic explanations in more common autoimmune diseases.

Primary complement deficiencies PCD are rare diseases that appear at any age with severe infections, autoimmunity, angioedema or asymptomatic.

They are probably vastly under diagnosed within clinical practice. In order to improve this situation, we developed a systematic study selecting patients according with preset inclusion criteria.

The diagnostic strategy includes functional complement assays for classical and alternative pathways and C3 and C4 quantification as first step and then measure of factors according prior results.

Sixteen patients were the index case but 6 appeared after family search. We notice the beginning of symptoms at early age with a delay at the first consult and diagnose.

It must be suspected a PCD in any patient with severe or recurrent infections by capsulated bacteria, with normal quantitative and functional antibody response, atypical autoimmune disease or recurrent non allergic angioedema.

An appropriated algorithm to study the suspected cases let identify the deficit, and propose the adequate therapy.

Garrahan During the past 15 years, the elucidation of the genetic etiology of an increasing number of primary immunodeficiencies allowed the application of mutation analysis as an integral part of the complete evaluation of these patients.

But a stepwise screening approach always ensures efficient and thorough evaluation of mechanisms of immune dysfunction that may underlie clinical presentation with narrowing diagnostic options, before using the molecular studies that may be required to arrive at specific diagnoses.

Firstly, not all of the patients with identical clinical and laboratory findings have mutations in the same gene, we must consider family history and additional screening tools to distinguish between several candidate disease genes before sequencing them.

In addition, we must be able to interpret when a mutation we found is actually a disease causing or a highly prevalent low penetrance mutation or even a single nucleotide private polymorphism.

Furthermore, genomic DNA sequencing, the standard approach used to characterize a possible gene mutation has certain limitations, and alternative follow-up approaches may be necessary to establish the molecular basis of the primary immunodeficiency in a given patient.

Case studies being illustrative of identification and resolution of these situations aiming to avoid misdiagnosis will be discussed.

Adriana T. Larregina Department of Dermatology, University of Pittsburgh School of Medicine Recurrent skin inflammatory diseases relay on the synchronized interaction of the immune and nervous systems which takes place during the process known as neuroinflammation.

Contact hypersensitivity, CHS and atopic dermatitis AD are prototype recurrent skin inflammatory diseases initiated and sustained by type-1 and type-2 biased T cell responses, respectively.

This inflammatory microenvironment of is initiated and controlled, at least in part, by neuropeptides. In the present lecture I will discuss the role and mechanisms employed by these two cutaneous pro-inflammatory neuropeptides regarding the regulation of skin chronic inflammatory diseases.

Breast milk immune complexes are potent inducers of oral tolerance in neonates and prevent asthma development Nicolas Glaichenhaus University of Nice-Sophia Antipolis, Valbonne, France Allergic asthma is a chronic lung disease resulting from an inappropriate T helper Th -2 responses to environmental antigens.

Early tolerance induction is an attractive approach for primary prevention of asthma. We have found that breastfeeding by antigen-sensitized mothers exposed to antigen aerosols during lactation induced a robust and long-lasting antigen-specific protection from asthma.

Protection was more profound and persistent than the one induced by antigen-exposed non-sensitized mothers. The induction of oral tolerance by milk immune complexes did not require the presence of transforming growth factor-beta in milk in contrast to tolerance induced by milk-borne free antigen.

Furthermore, 21 neither the presence of IgA in milk nor the expression of the inhibitory Fc-gamma-RIIb in the newborn was required for tolerance induction.

This study provides new insights on the mechanisms of tolerance induction in neonates and highlights that IgG immune complexes found in breast milk are potent inducers of oral tolerance.

Neutrophils, however, have, upon activation, considerable potential to cause collateral damage and harm host tissues, in particular through the release of numerous proteases such as neutrophil elastase NE , cathepsin G, proteinase-3, metalloproteases, cysteine proteases It seems therefore important for the host to protect itself by producing antiproteases.

Our presentation will present some of the most recent data in that field. Recent evidences suggest that their function is not solely restricted to chemotaxis, but also participate in many other immune functions such as dendritic cell maturation and T cell activation and differentiation.

CCL18 is a chemokine expressed in lung and lymph nodes, has an unknown receptor, is produced by antigen-presenting cells and is up-regulated by Th2 cytokines.

Conversely, this property was lost in allergic subjects in association with a decreased binding of CCL18 to its putative receptor.

Buenos Aires, Argentina Biofilms are microbial communities enclosed in a polymeric matrix adherent to inert or living surfaces.

Compelling data indicate that biofilms are structurally and dynamically complex biological systems that are crucial in the pathogenesis of many clinically important bacterial infections.

Neutrophil are essential immune effectors in the first line of defense against bacterial infections. In previous studies we determined that immobilized-eDNA also activates neutrophils.

Our new findings, based on experiments performed with P. Biofilms formed by a P. Assays with biofilms formed with mucoid P.

We conclude that eDNA immersed in the matrix of bacterial biofilms is a major proinflammatory component of P. Osteoarticular Brucellosis: inflammation, matrix metalloproteinases and induction of osteoclastogensis.

Brucella can infect and survive within human osteoblasts and this infection elicits the secretion of chemokines IL-8 and MCP-1, attractants for neutrophils and monocytes, respectively that might be involved in the osteoarticular manifestations of brucellosis.

The recruitment of phagocytes may enhance the immune response since these cells can be activated within the infection focus to secrete additional inflammatory mediators.

In particular, macrophages in inflamed tissues can differentiate not only to osteoclasts the only cells known so far to be able to degrade bone , but they also appear to accelerate bone resorption through the production of proinflammatory cytokines and matrix metalloproteinases.

On the other hand, monocytes in inflamed tissues can also accelerate bone resorption by differentiate to osteoclast, in a way that involved, B.

These results suggest that proinflammatory responses elicited by B. Alberto L. The number of host genes involved in the implementation of adaptive immunity and in the execution of constitutive and inducible innate defensive mechanisms against viruses is vast.

Likewise, pathogenic viruses have evolved many different self-protective mechanisms that operate to mask their presence within the organism and to disrupt the host defences.

The outcome of this struggle is that the hosts will generally prevail at the level of the whole organism, thus resulting in host survival, while lytic viruses will win the intracellular battle, thus warranting virus survival and spread.

The ability to counteract host responses is, however, a feature of wild-type viruses only. Viral vectors are artificial entities that have been developed to deliver therapeutic transgenes and, therefore, the transduced cells should be preserved alive.

Towards this end some viral genes are often inactivated, resulting in a breakdown of the vector ability to survive in the infected cells.

The vector genome will consequently be silenced or eliminated, which constitutes a major hurdle hampering the use of vectors in gene therapy.

This talk will summarize current evidence underlying these concepts, using HSV-1 as model, and will speculate on possible ways to counteract the host defences, allowing stable and safe transgene expression.

As most pathogens infect mammals by respiratory, digestive, urogenital tracts, these specialized barriers are thus essential sites for anti-microbial immunity.

The innate immune response to bacterial flagellin, a molecular pattern specifically expressed in mucosa, is mediated by TLR5, which is expressed on various sentinels like epithelial or dendritic cells.

The presentation will focus on mucosal immunes responses induced by the TLR5 signalisation by two experimental models: 1 a systemic administration mimicking pathogen invasion in mucosal tissues and 2 a local administration mimicking microbial colonization of mucosa.

We will present data demonstrating that sentinel cells and effectors mechanisms are different in these models.

Persistent viruses including human immunodeficiency virus HIV , hepatitis B virus HBV and hepatitis C virus HCV infect more than millions people globally causing severe clinical symptoms and high mortality.

Because human persistent viruses are heavily host-restricted in most part to humans and non-human primates , we used lymphocytic choriomeningitis virus LCMV infection of its natural host, the mouse, as a model system to study the interactions between the immune system and the pathogen during in vivo chronic viral infection.

We have uncovered unique cytokine profiles throughout the course of the infection and evaluated their biological effects at the molecular, cellular and whole organism level.

Our data support the overall conclusion that the host immune system is dysregulated or re-educated to coexist with the persistent virus and provide new insights into the parameters governing the conditioned immune responses during chronic viral infections.

Thus, activated specific T lymphocytes display a crucial role in the immune response of the host to the pathogen. Actually, it was demonstrated that IL produced by CD4 T cells would be required to eliminate primary Mtb infection and to establish an effective memory response.

In this regard, we have demonstrated that tuberculosis patients display higher number of Treg cells compared to healthy donors. Furthermore, patients with active disease produce higher levels of IL than healthy controls.

These cells produce large amounts of IL-9 in response to the pathogen. Thus, during active tuberculosis, Tregs, Th1, Th17 and Th9 cells would be required by the human host to fight Mtb.

Influence of Mycobacterium tuberculosis genotypes on the host immune response. Maria del C. Sasiain Academia Nacional de Medicina, Buenos Aires, Argentina 24 The influence of strain variation on the outcome of infection and on the immune response induced by Mycobacterium tuberculosis is a nascent area of research.

Unlike many bacterial pathogens, gene exchange is rare in M. Our research projects are focused on the ability of the most prevalent strains causing sensible or multidrug-resistance MDR tuberculosis in Argentina.

We are working on the innate and the adaptive immune response developed by these strains in latent infected and in tuberculosis patients.

In general, Haarlem strains are lesser immunogenic than LAM strains. Hence, it should be considered the dependency on M.

Understanding the interactions of the bacilli with the host immune system could help to develop specific and more efficient treatments.

Dendritic cells DCs are thought to play a major role in initiation of immune responses to intracellular pathogens, in part through their production of the important pro inflammatory cytokine IL In the case of infection with the intracellular protozoan T.

The ability of the tumour microenvironment to alert the innate immune system has been a long lasting question and debate.

Plasmacytoid pre-dendritic cells pDCs have a special position in linking innate and adaptive immunity. They are dedicated to the production of type I IFNs after the recognition of viral and microbial products.

TLRindependent activation of pDCs may be involved in conditions of sterile inflammation. Our results show that cytokines can act as tumour-derived endogenous danger signals that alert the immune system through they effect on pDCs.

Cancer immunosurveillance appears to be an important host protection process that inhibits carcinogenesis and maintains regular cellular homeostasis.

Cancer would develop in the rare occasion when tumor cells escape that immune response. This quite old and widely accepted paradigm has surprisingly resisted the accumulation of contradictory evidences, like i the understanding of the molecular mechanisms of carcinogenesis that makes impossible that we constantly generate cancer cells or i the fact that long-term immunocompromised patients do not have increased incidence of non-viral induced cancers.

There is an immunosurveillance of cancer, but one that depends on the memory status of the players. In the normal setting, cancer immunosurveillance is mediated by regulatory T cells that protect rather than eliminate cancer cells; in a pre-immunized setting, cancer immunosurveillance is mediated by memory effector T cells that eradicate tumor cells.

This explains another old paradigm of cancer immunology, that preventive immunization is much more effective than therapeutic immunization.

These results have significant therapeutic implications and notably should prompt to reconsider preventive vaccination against cancer. The microenvironment of human tumors differs, from patient to patient in their lymphocytic infiltration.

In addition, lymphocytes are not randomly scattered within the tumor but appear organized in the center of the tumor, its invasive margin and in tertiary lymphoid follicles adjacent to the tumor nests.

We have particularly analyzed large cohorts of colorectal and lung cancers and shown that the infiltration of memory T cells, with a Th1 and cytotoxic orientation, both in the center and the invasive margin of the primary tumors is a major prognostic factor since it controls tumor recurrence, probably through an immune control of potential metastatic cells.

These data allow to draw an integrated picture of how an immune reaction develops in the tumor microenvironment to control cancer spread and recurrence.

Universidad Nacional de Cordoba, Argentina. Toll-like receptors TLRs recognize molecules derived from pathogens as well as endogenous danger signals possessing similar chemical structures.

Administration of their ligands to activate antigen presenting cells has always been considered a valuable tool to promote anticancer immunity.

Interestingly, the presence of functional TLRs in cancer cells has been demonstrated, raising the question about the role that these TLRs could be playing in tumors.

We have reported that B16 murine melanoma cells as well as other tumor cell lines stimulated in vitro with a TLR4-ligand during 48h prior to their inoculation into TLR4 deficient mice TLR4lps-del , induce tumors significantly smaller than controls.

A transitory halt of tumor growth was observed in TLR4 26 deficient animals which were intratumorally treated with LPS, indicating that TLR4 present on tumor cells could positively contribute to tumor growth control.

The apoptosis-proliferation balance of LPS-stimulated B16 cells is not modified and inhibition of tumor growth was not observed in nude mice; thus we hypothesized that TLR4 triggering on B16 cells themselves could induce the expression of pro inflammatory mediators, that even if they are transitory, could dramatically alter the function of dendritic cells DCs present at the site of inoculation and switch the type of immune response elicited against the tumor.

Transcriptional analysis as well as cytokines secreted show that TLR4 triggering on B16 cells induces changes in important DCs modulators.

Our results open up new avenues for understanding the role of TLR4 in tumor cells and for identifying potential new therapy strategies for cancer.

High-risk human papillomaviruses HPV are the main etiological agent of cervical cancer, the leading cause of cancer death among women in low-income countries.

Furthermore, they are also highly associated with the development of others anogenital and oropharyngeal carcinomas. Commercially available prophylactic HPV vaccines were shown to be ineffective on pre-existing neoplastic processes, thus having no immediate impact on the actual incidence of HPV-related cancers.

HPV E7 and E6 early oncoproteins represent ideals targets for immunotherapeutic intervention due to their key role in cellular transformation and constitutive expression in HPV-associated tumors.

Recently, we have developed a recombinant E7-based vaccine, exhibiting strong immunotherapeutic properties in a well established HPV tumour model.

Vaccination of female mice with low doses of the recombinant HPV E7vaccine totally prevented tumour outgrowth, even after a 3 months rechallenge.

Therapeutic treatment of tumour-bearing mice with the vaccine-type molecule also shows a remarkable activity, completely reverting the tumor growth.

These proof-of-principle experiments demonstrate the potential applicability of our vaccine candidate to the treatment of HPV-related neoplastic lesions.

Michel Braun Institute for Medical Immunology. However, this approach has fallen short of expectations, because T cells chronically stimulated by persistent antigen often become functionally exhausted and thus do not respond appropriately to therapeutic vaccination.

On the contrary, in transplantation, immunosuppression of acute rejection is known to induce chronic pathologies in the allograft, and controlling the activity of chronicallystimulated alloreactive T cells is one major problem currently facing immunologists.

Therefore, understanding the biology of T cells chronically stimulated by persistent antigens is essential to the development of therapeutic strategies that could control many immunological disorders.

We have studied a mouse model where persistent stimulation of CD4 T cells led to multi-organ T cell infiltration. Exposure to systemic antigen, however, deeply modified T cell function and chronically stimulated T cells developed a long-lasting state of unresponsiveness, or immune adaptation, characterised by their inability to mediate organ immune damages in vivo.

However, analysis of the gene expression profile of adapted CD4 T cells revealed the specific co-expression of genes known to promote differentiation and function of Th1 effector cells as well as genes coding for proteins that control T cell activity.

Our work aims at the identification of the molecular mechanisms responsible for the phenomenon of T cell immune adaptation to persistent antigen.

These cells account for a durable Tcell reconstitution, generating a diverse TCR repertoire and robust response to infections.

Renal transplantation may be affected by immediate injury during post-transplantation period as a result of immunological and non-immunological causes.

The two most important determinants of non-immunological injury are ischemic and reperfusion injury and brain death. Both lead to delayed allograft function, acute rejection, and diminished graft survival in the long term consequently increasing transplant costs.

Better antibody detection tests have been developed and, as a result, hyperacute rejection is now extremely rare.

In addition, different options as induction therapies have improved acute rejection rates during the first year after transplantation.

Allograft long term survival rates have not improved significantly. The development of anti- HLA antibodies, especially class II, is the main cause of transplant glomerulopathy.

This entity causes allograft chronic dysfunction. Rabinovich, Juan M. Ilarregui, Diego O. Croci, Mariana Salatino, Marta A.

Toscano, Victoria Sundblad, L. Mascanfroni, Juan P. Recent efforts toward decoding the glycosylation signature of immune cell processes have revealed dramatic changes during T cell differentiation.

These alterations are also detected during the course of dendritic cell maturation, suggesting that protein-glycan interactions may have a decisive role in the control of immune cell responsiveness and tolerance.

Blockade of galectin-1 expression results in heightened T-cell-mediated tumor rejection. Moreover, galectindeficient mice exhibit augmented TH1 and TH responses and are considerably more susceptible to immune-mediated fetal rejection and autoimmune disease than their wild-type counterparts.

Yet, the mechanistic bases underlying these anti-inflammatory effects are still uncertain. We will discuss the identification of a circuit linking galectin-1 signaling, generation of tolerogenic dendritic cells and expansion of regulatory T cells which contributes to the resolution of autoimmune inflammation and modulates T cell responses in antigen-specific and neoplastic settings.

Finally, we will highlight the role of these lattices in linking tumor hypoxia to neovascularization.

As in peripheral organs, multiple TLRs are dynamically expressed appear to play important roles in both tissue surveying and repair, and are involved in mounting a host-defense response against microbial invasions.

The immune and inflammatory response that follows can either benefit the host or further contribute to pathology.

This study explores the effect of TLR agonists on the CNS and uses New World arenavirus Tacaribe, a neurotropic pathogen that is lethal in newborn mice, to explore the role of TLR-mediated innate immune responses in disease pathogenesis and treatment.

Our studies demonstrate that the TLR immune activation pathway is required for the pathogenesis of Tacaribe.

Protection was mediated by an increase in antigen-specific antibodies IgG and IgM and required inducible nitric synthase iNOS expression and nitric oxide NO production.

Biological Chemistry Dept. The pathogenic mechanisms of disease are presently unknown and the active involvement of epithelial acinar cells producing inflammatory mediators in the induction and perpetuation of the inflammatory response supports its characterization as an autoimmune exocrinopathy.

The hypothesis of an impaired balance of neuroimmune interactions in the target organ at the onset of the disease can be approached in the non-obese diabetic NOD mouse model of SS.

At the pre-diabetic stage, NOD mice have the unique characteristic of developing a deep secretory loss with mild infiltration of the glands consistent with a structural-dysfunctional aetiology.

In keeping with a defect in salivary gland homeostasis as initial trigger of the autoimmune exocrinopathy, an enhanced apoptosis of acinar cells and reduced salivary secretion and signaling upon vasoactive intestinal peptide VIP stimulation was observed.

VIP is a neuro- and immunopeptide that promotes exocrine secretion, contributes to vasodilation in exocrine glands and induces anti-inflammatory effects through its action on macrophages.

On this basis, we are currently exploring the role of apoptotic secretory epithelium as a pro-inflammatory triggering factor of exocrine dysfunction in the NOD model of Sjogren's syndrome and the modulatory effect of VIP on the dialogue of acinar cells and macrophages.

T1AD is multifactorial in origin with both genetically and environmental determinants conferring susceptibility to disease onset. Agents that fulfill these qualities have potential for therapeutic use, and might induce tolerance in autoimmune diabetes and islet transplantation.

We have recently described strong experimental evidence of the employment of galectin-1, a soluble lectin, able to restore immune balance in T1AD mouse models by means of different mechanisms.

Following a similar rationale we are now searching for novel compounds and combinatorial therapies without unacceptable risks associated with continuous immune suppression to control the autoimmune burden of T1AD and hopefully, reaching permanent arrest of autoimmunity.

DNA recognition by antibodies is at the center of autoimmune disease, in particular, in Lupus Systemic Erythemoatosus SLE , where 9 out of 10 patients are females and no specific treatment is available.

Although suspected, there is no clear proof that DNA is the actual immunogen is DNA, however, the pathogenic antibodies that cause tissue damage recognize DNA and are in fact a hallmark for the disease.

Our lab has been investigating the molecular basis for antibody-DNA recognition. We had obtained high affinity sub-nanomolar and specific monoclonal antibodies.

We present an integrated mechanistic analysis, combining structure, thermodynamics and kinetics. Our model system is the only antibody-nucleic acid recognition out of a handful which: i antibodies were elicited by a specific a known DNA immunogen and ii have an integrated mechanism dissected with fold higher affinity.

These studies should open the posibility of combining basic research of a well described model with clinical research, comparing binding behaviour with sera antibodies from patients, and possible diagnostic applications.

More importantly, even considering that SLE is known to arise from a complex combination of genetic, environmental and other factors, our studies may constitute the basis for drug screening and design of therapeutic compounds that can block pathogenic anti-DNA autoimmune antibodies.

School of Medicine. Catholic University of Cordoba. Giardia lamblia is a human intestinal pathogen. Recently, we found that the mechanism controlling variant-specific surface protein VSP switching in Giardia involves components of the RNA interference machinery, and that disruption of this pathway generate trophozoites expressing simultaneously many VSPs.

Here, we utilize these altered trophozoites to determine the role of antigenic variation in an animal model of giardiasis. Our results show that either primary infection with trophozoites expressing all VSPs, or immunization with purified VSPs from the transgenic cells, protects animals from subsequent Giardia infections.

These results constitute the first experimental evidence that antigenic variation is essential for parasite survival within hosts and that artificial disruption of this mechanism might be useful in generating vaccines against important pathogens that exhibit similar behaviour.

Facultad de Medicina, UBA. Argentina 31 It has been almost 30 years since the detection of the first HIV-1 cases and yet an effective and safe vaccine has not been developed.

One of the challenges to address and ultimately overcome when developing a vaccine is the high variability of HIV Studies performed in our laboratory analyzed the impact of the immunogenicity of BF recombinant variants in the design of future vaccines employing Nef and Env proteins as a model.

After prime-boost immunizations we found that a cellular response of high specificity with low cross-reactivity against subtype B was generated.

We analyzed the peptides involved in the specific and cross-reactive responses, as well as potential immunization strategies to cover the immunogenic epitopes targeted after the single B and BF immunizations.

These results will be pivotal for our region, indicating that antigens from BF viral variants must be considered for a future vaccine.

Cargnelutti1,2; M. Lacoste1,2 ; G. Rabinovich3,4 ; M. Yersiniosis is a zoonotic foodborne associated with a risk ReA. It belongs to the group of arthritidies known as the spondyloarthropathies SpA.

The pathogenesis of ReA is incompletely understood. Accordingly, IL levels were increased in synovial fluids of SpA compared with control osteoarthritis patients.

Cazorla, Fernanda M. Frank, Marina N. Matos, Carolina Ramirez, Emilio L. Several vaccines against Chagas disease have been studied; however, all vaccination regimens tested so far conferred partial immunity.

Despite the strong immune response elicited by vaccination, the parasite survival suggests that, similarly to what happens in natural infection, the immune response is either insufficient or inherently inadequate.

The major cystein proteinase, cruzipain Cz , has a catalytic domain and a C-terminal extension.

Although the role of the later domain is unknown, is the major immunogenic part in infected humans. Immunization employing full-length rCz or its N- and C-terminal domains demonstrated that the C-terminal domain allows Cz to circumvent the immune response to the catalytic N-terminal.

This is a property of the molecule itself, since inoculation of rCz produces a similar effect than Cz in natural or experimental infection.

Cz is not the only T. In addition, we demonstrated that by immunizing with the N-terminal domain alone, it is possible to differentially orient the host immune response providing a better protection than that elicited by full-length Cz.

This observation has an important implication in terms of optimizing a rational vaccine design. The parasite expresses trans-sialidase, an enzyme that transfers sialyl residues among glycoconjugates and sialylates the surface components.

The enzyme is also shed to the bloodstream. Sialyl residues incorporate strong negative charges to the glycoconjugates and are involved in several biological functions.

Therefore, the trans-sialidase-induced alterations of sialylation patterns are associated with several abnormalities observed during the infection.

In fact, the strong thymocyte depletion and the absence of germinal centers in secondary organs, together with thrombocytopenia are prevented by the passive transfer of a trans-sialidase-neutralizing mAb to infected animals.

Incorporation of the sialyl residue leads CD4CD8 thymocytes to enter apoptosis, whereas its removal induces thrombocytopenia. A major obstacle to understand these events was the difficulty to identify the transferred residues among all those naturally occurring.

This limitation was abrogated by an unnatural sugars approach, because trans-sialidase efficiently hydrolyzed and transferred azido-sialic acids to lymphocyte surface where CD45 and integrins were identified as acceptors.

Then, trans-sialidase provides both a suitable target for chemotherapy and a tool to explore the glycobiology of the immune system.

The liver was the most affected tissue with numerous cellular infiltrates, apoptotic cells and necrotic areas.

Infection increased transaminase activities in both mouse strains, although they were highest in B6 mice. To gain insight into the molecular basis, we investigated the TLRs commitment in hepatic tissue.

We found a different modulation of TLR2, 4 and 9 in this tissue, associated with an intensified proinflammatory cytokine profile in B6. Notably, Pam3CSK4 TLR2-agonist treatment, previous to infection, induced a significant reduction of transaminase levels and inflammatory foci in liver of B6 mice.

Proinflammatory cytokines were decreased and TGFb increased by B6 purified hepatic leukocytes. Our results describe some of danger signals involved in liver response and clearly demonstrate that Pam3CSk4, previous to infection, can attenuate the exacerbated hepatic inflammation.

After the invasion process, trypomastigotes are temporally contained in a membrane vesicle known as the parasitophorous vacuole TcPV.

Subsequently the parasites escape to the cytoplasm and differentiate into amastigotes replicating actively. Host cell invasion is governed by trypomastigotes-triggered activation of host cell signaling pathways.

At least two main invasion process have been described: the calciumdependent recruitment and fusion of lysosomes with the host plasma membrane, and the activation of a class I PI 3-kinases that leads to the invagination of the plasma membrane generating a vacuole initially devoid of lysosomal markers.

Work from our laboratory indicates that the TcPV is decorated by the autophagic protein LC3 33 and that that autolysosomes are recruited to T.

Interestingly, activation of autophagy before infection significantly increased the number of infected cells whereas inhibitors of this pathway reduced invasion.

In addition, the absence of critical proteins required for autophagosome formation, limited parasite entry. These results indicate that mammalian autophagy is a key process that favors the internalization of T.

We observed that expression of FOXP3 in activated PBMCs was already present above baseline before any cell division, indicating that was induced in cells that were previously negative for this transcription factor.

Finally, those conditions in which iTregs may play a central role can be associated with the expansion of Tregs observed in the pre-implantation phase of the menstrual cycle and during pregnancy.

Intriguingly, in contrast to many cell types, skeletal muscle fibers do not physiologically express detectable levels of major histocompatibility class I MHC -I molecules.

This model revealed that tolerance to muscle autoantigens implies ignorance for CD4 and, presumably, peripheral deletion for CD8 T cells.

In contrast to other autoimmune models based on tissue-specific expression of a neo-autoantigen, transfer of anti-Ova T cells to SM-Ova mice did not lead to myositis while Ova-bearing tumors were rejected, presumably because of lack of muscle MHC-I expression.

It was known that induction of muscle H-2Kb expression in iMHC Tg mice provokes a severe myopathy, seemingly through the presentation of cryptic muscle autoantigens to autoreactive T cells.

Proteomic analysis evidenced up-regulation of chaperonins and UPR proteins characteristic of endoplasmic reticulum stress.

Hence, expression of H-2Kb by muscle fibers may be pathogenic per se. Many host-reactive T-cells were identified but they were anergized in these human chimeras.

Responses in vitro and in vitro antibody production, cytotoxic activity against virus-infected target cells were extremely effective despite the lack of HLA molecule shared between T-cells and all other cells of the body.

The differentiation of stem cells into mature Tcells in the context of a foreign host thymus therefore led to the selection of T-cell recognition structures of a peculiar type.

Morelli T. Starzl Transplantation Institute. University of Pittsburgh, Pittsburgh, PA. During the past decade, there has been a shift from the perception of dendritic cells DCs solely as professionalantigen Ag -presenting cells APCs capable of inducing immunity to the view that these cells are also crucial regulators of tolerance.

Most of the current DC-based methods to induce donor-specific immunosuppression for transplantation rely on the passive transfer of in vitro-generated DCs rendered immature, maturation-resistant MR- or alternatively-activated by pharmacological or genetic manipulation.

However, this simple idea has not been tested in vivo. The effect on the anti-donor response was independent of the method used to generate therapeutic DCs or their viability, and in accordance with the idea that recipient APCs mediate the effects of therapeutic DCs in transplantation, prolongation of allograft survival was achieved using donor apoptotic MR-DCs or those lacking surface MHC molecules.

In conclusion, our findings indicate that DC-based therapies modulate the anti-donor response through recipient APCs and that the systemically injected immunosuppressive DCs function as Ag-transporting cells rather than APCs to prolong allograft survival.

Comparing efficacy in larger animal models is yet to be performed, and our study does not preclude future generation of immunosuppressive DCs capable of directly mediating T cell suppression.

But given the cost, time and risk of DC-based therapies, our data raise some concern on the potential benefits of current DC-based therapies in transplantation over previously tested and simpler methods like donor-specific transfusion.

Universidad de la Republica. Montevideo, Uruguay. Different parameters are critical to engineer tolerogenic dendritic cells Tol-DCs to be used as therapeutic tools to manipulate antigen-specific immune responses.

Injection of autologous Tol-DC same strain than the recipient is able to prolong allograft survival significantly. Although the reasons of this difference have not been established, autologous Tol-DC imply practical advantages to be used in a clinical setting.

When autologous TolDCs not pulsed with donor antigens are associated to sub-optimal immunosuppression, a synergistic effect is 35 achieved, leading to donor-specific allograft tolerance.

We will discuss the immunological mechanisms of this effect and the advantage to use autologous tolerogenic dendritic cell therapy in organ transplantation.

We will treat the reasons why this is a clinically relevant approach and the experimental data that support this strategy.

The Tn Ag is expressed on human carcinoma-associated mucin variant and has attracted increasing interest in clinical oncology since it is widely expressed in a variety of adenocarcinomas.

Intradermal immunization with MAG:Tn3 induced high levels of Th2 cytokines and anti-Tn antibodies recognizing human tumor cells.

This meeting was possible thanks to the Argentine and French Immunological Society, especially to Dr. Eduardo Chuluyan and all the professionals that have been invited to this important Congress.

Daniela Di Giovanni, who worked hard with me to make this event possible. Since we have began a hard and long struggle against many obstacles we found in the way in the every day routine; making diagnosis and treatments for patients with immunodeficiency diseases.

In the last ten years the development of the Clinical Immunology let us get better diagnoses and treatments and good evolution in our patients.

We could make a question to ourselves: Why? What kind of the Immunology do we really want? What kind of medicine do we want?

This is a fundamental question that most of us are asking? Does it make sense to participate in the existing world order? We want a world where life is preserved, and the quality of life is enriched for everybody, not only for the privileged.

But our way is very long, there are lots of thing to do and we feel very lonely in this battle, because we receive little help from our government and some private laboratories.

In Argentina small group of professional and foundations are doing what they can do with a few tools but with passion. Passion lives here.

Heart is what drives us and determines our fate. I would like for the people who works with health, people who ask questions, who bend the rules and take risks, people like all of you in this room.

In our country a young group of doctors, biochemical and Parents Society are working together to spread all the information they get about IDP.

More than Highly dynamic interactions of phagosomes, first with endosomes and then with lysosomes, lead to the maturation of phagosomes into phagolysosomes.

Contrary to others phagocytes, which degrade ingested particles to amino acids, dendritic cells only partially degrade ingested proteins, preserving protein fragments that associate to MHC molecules for the onset of adaptative immune responses.

To do so, dendritic cells have developed a specialized phagocytic system, different from that of other phagocytes, such as macrophages or neutrophiles.

In contrast to other phagocytes, which acidify their phagosomes very actively, dendritic cells maintain a neutral or slightly alkaline pH in phagosomes.

In addition, dendritic cells phagosomes present several other unique functional specializations, including the capacity to export phagocytosed molecules to the cytosol or to recruit ER resident proteins.

In order to further understand the role of these phagocytic specializations in cross presentation, we have analyzed the molecular mechanisms involved.

Using shRNAmediated knock-down of different proteins, we have evaluated the role of ER-recruitment to phagosomes in cross presentation. Our studies show that dendritic cells have developed a specialized phagocytic pathway, highly adapted to their main function, the presentation of phagocytosed antigens for the initiation and the control of adaptative immune responses.

This metabolic pathway is responsible for reactive oxygen species generation during respiratory burst, then associated to germ killing within phagocytic cells, and inflammatory reactions.

CGD patients typically suffer from two types of clinical manifestations: recurrent bacterial and fungal infections, and dysregulated granulomata formation.

Early diagnosis, antimicrobial prophylaxis, and aggressive management of infectious complications are the cornerstones of CGD management.

These three measures have strikingly improved life expectancy and quality of life in the last fifty years. Interestingly, very encouraging and promising results have been lately achieved with definitive and curative options for this disease.

Besides, new aspects regarding genetic pathophysiology, genotype-phenotype correlation, microbiological susceptibility, and new potential therapeutic approaches will also be discussed.

Antibodies associated to autoimmune disease and B cell compartment in pediatric patients with Chronic Granulomatous Disease.

The recurrent infections are the result of this 37 defect. Also are observed abnormally exuberant inflammatory responses leading to granuloma formation such as granulomatous enteritis, genitourinary obstruction.

In 10 CGD patients pts ,mean age: 11 years, range: 3 X-linked -gp91phox, 5 autosomal recessive 4 p47phox; 1 p67phox and 2 with no molecular diagnosis, half of them with some gastrointestinal involvement, we evaluated the prevalence of different antibodies associated to autoimmune diseases and characterize peripheral B cell compartment and correlate with clinical features of CGD.

We found high prevalence of ASCA in our CGD pts as has been reported in inflammatory bowel disease, but do not know what the real clinical value in these pts.

Most our CGD had B cell compartments defects with normal functional antibody response. In our follow-up on that the defect in B cells is only phenotypic.

It would be interesting to evaluate regulatory pathways that control B cell differentiation, which could be implicated in this phenomenon.

We describe unrelated patients with mycobacterial disease and a dominantnegative IRF8 allele. Autosomal dominant IRF8 deficiency is therefore a novel genetic etiology of mycobacterial disease.

Despite Mendelian inheritance in most cases, mutations of a given gene can lead to a variable expression of the corresponding disease.

Somatic mutations can be a key event in this process, either by reverting a profound inherited defect or by strengthening a partial deficiency.

Reversion mutations were described in numerous cases and restored the impaired expression or function of a gene product, thereby leading to an attenuated clinical phenotype.

In most cases, ALPS is the consequence of germline mutations with partial clinical penetrance. We now found in families carrying mutations 38 with low clinical penetrance that combined germline and somatic mutations of the FAS gene could account for the onset of ALPS in patients, whereas carriers of only the germline mutation remained asymptomatic.

This observation illuminates the impact of somatic mutations in the expression of ALPS and may have further implications in the phenotypical variability of some primary immunodeficiencies or in the onset of other autoimmune diseases.

The national registry did not distinguish data between from different centers and we did not have more processed information than it was published.

While we are registering all immunodeficient patients again, we still do not have any processed information from it. So we have to show the analyzed data of our group as recorded by ouerselves.

From the creation of the Group in until , we had primary immunodeficient patients. Since our group has had out of these were classified according to the IUIS classification.

We think that the great increase in the number of patients with immunological diagnosis in the last three years is mainly due to more than one cause.

Finally, we emphasize the importance of an Argentinean registry for the Argentinean patients. Three Centers experience: A model for patient care in pediatric immunology in Rosario Dr.

Within this net, the ICP unit, carries out different activities which involve professional training and lecturing.

During January June , patients were diagnosed with PID as follows: antibody deficiencies Others: familial haemophagocityc lymphohistiocytosis 3 patients and citophagic histiocytic panniculitis 1 patient.

Bringing the ICP unit into the Health Care System has allowed an early detection and derivation of patients suspected of having some kind of immunological disorder, it has also allowed a more efficient use of existing health care resources and an adequate use of other services.

Our goal was to know the incidence and prevalence of primary immunodeficiencies PIDs and their frequency.

The PDI represents a low percentage of the general pathology and the information obtained in the registry increases the chances for early diagnosis and treatment and reduces morbidity and mortality.

One Center recording in La Plata Dra. In the last years the hospital has produced 14 discharges per year. The creation of the Immunology Unit dates from and consists of an outpatient, a day hospital care and a hospitalization area.

There is also a bone marrow transplant unit as part of the Hematology Service. Since there have been registered patients with primary immunodeficiency PID.

The distribution is the following: patients with antibody deficiencies Other PID diagnosed were 5 patients with granulocyte defects 1.

The remaining patients are diagnosed with: familial lymphohistiocytosis 0. Although there is a correlation with international registrations, we have a slight underreporting in SCID probably due to the severity and early death in these children.

Bruton recognized that an eight-year-old child with a four-year history of many serious septic episodes was incapable of making significant quantities of immunoglobulin.

The first congenital agammaglobulinemic patient was diagnosed. After that many primary immunodeficiencies PID have been described.

Recurrent bacterial infection is the hallmark of humoral primary immunodeficiencies PID. These patients suffer from life-threatening infections, and the goal standard of their treatment is the prevention of infections.

The need for immunoglobulin Ig replacement therapy was and still remains the mainstay of therapy not only for humoral PID but for some combined T and B-cell immunodeficiencies and for many others PID.

The first available route of immunoglobulin infusion was intramuscular but it was painful and adequate IgG levels were difficult to reach. After that, Ig replacement therapy has evolved considerably.

Today, many products are available and suitable for intravenous or subcutaneous administration. Individual catabolic rates of administered IVIG should be considered and higher doses may be important in those patients who have stablished lung disease.

Adverse events, such as headache, backache, chills, fever, chest tightness, are generally mild, and respond to anti-inflammatory, antihistaminic or adjustment of the infusion rate.

Serious adverse events are extremely rare. Also subcutaneous immunoglobulin administration can be recommended which could be performed by the own patient at home.

This provides stable IgG levels. IVIg has a number of important uses in the treatment of disease. Initially used as a replacement therapy for patients with primary and secondary immunodeficiency diseases, IVIg is now widely used for a number of autoimmune and inflamatory diseases.

IVIg exerts two major modes of action: antigen specific activity and immunomodulation. Many progress has been made in undestanding these mechanisms.

The mechanisms of action of IVIg are complex, involving modulation of expression and function of Fc receptors, interference with activation of complement, the cytokine network and idiotype network.

IVIg targets the cellular immune compartment at multiple levels, including innate and adaptative immune cells. Once these patients begin receiving IVIG on a regular basis their health status improves markedly.

This treatment reduces the frequency and severity of infection, days of antibiotic usage and hospital admissions.

Previous studies support that, in general, higher doses of gammaglobulin and higher serum levels are associated with fewer infections.

Late diagnosis and delayed of IVIG replacement therapy result in increased morbility and mortality.

The cost benefit for IVIG treatment among patients with PIDD would be higher if these ones did not suffer permanent organ damage prior this diagnosis and treatment.

Therefore we need to lead our efforts to obtain these data and to compromise health authorities in the promotion and supporting the access to gammaglobulin for PIDD patients treatment with antibody deficiency.

In experimental bone marrow transplantation, Tregs were described to be present among conventional T cells within the transplant and their depletion from the transplant before infusion leads to significantly accelerated graft versus host disease GVHD in different models, Thus, Treg elimination from DLI could be a way to improve alloreactivity and the associated-GVL effect in patients that relapse from hematological malignancies after HSCT.

In this study, we have compared in human two ways of Treg elimination and their consequences on the alloreactivity of the remaining T cells.

For the second one, we developed a strategy of positive selection of CD expressing-cells that excludes the Treg subpopulation.

Antigen cross presentation has been involved in establishing cytotoxic immune responses against bacteria, tumors and certain virus that do not infect DCs.

The presence of Endoplasmic Reticulum ER components in phagosomes has been proposed to be important for cross presentation.

However, there is no evidence about the mechanism of recruitment of these ER components to the internalization pathway. There is also no direct evidence that the ER recruitment to phagosomes is required for cross presentation.

We also observed that ER-deficient phagosomes acquire more rapidly lysosomal markers and display a higher proteolytic activity than normal DC phagosomes.

Our results suggest that the fusion of the ER to phagosomes is essential for cross presentation not only by contributing with the MHC class I presentation machinery, but also by delaying phagosome maturation and promoting cross presentation conditions.

Thus, activated specific T lymphocytes display a crucial role in the immune response of the host against the pathogen.

Moreover, the increase in IL-9 levels correlated with a significant increment of PU. Evaluation of new antigens for the diagnosis of latent M.

However, these tests cannot adequately differentiate between LTB and active disease. Thus, other latency antigens are currently under investigation to improve those clinical assays.

Therefore, the main objective of this work was to identify potential specific Mtb antigen candidates to be used in improved diagnosis assays.

However kinetics of this response revealed differences in its profile that may influence the outcome of the humoral immune response. Moreover, it has been recently suggested that IL might also contribute to the resolution of tuberculosis.

Then, in this investigation we studied the role of SLAM activation on the regulation of the cytokine milieu in tuberculosis.

Taken together, our present results suggest that SLAM activation leads to the generation of a complex cytokine microenvironment during active tuberculosis, having a crucial role in the homeostasis of the host immune response against the bacteria.

Low specificity high-false positive rates and standardization problems remain to be major controversial issues. The others populations consisted of 9 patients with venous thrombotic events, 20 with arterial thrombotic events and 19 patients with pregnancy morbidity.

Liposomes are lipid-bilayer vesicles that have emerged as a promising new adjuvant technology: effective antigen-deliver systems that serve to markedly enhance the uptake and presentation of APC.

Moreover splenocytes of immunized mice were isolated, and cytokine secretion was determined in presence of OVA. Also significant DTH response was observed these mice, specialy with cationic formulations.

Presence of liposomes induced specific Th1 and Th2 cytokine secretion in the spleen. These responses are crucial for vaccines that are required to protect against infection by a number of pathogens.

Thus, these alternative adjuvants would contribute to improve new generation vaccines, designed with recombinant peptides or proteins for generation of effective humoral and cell-mediated immune response.

Activated T cells from CLL patients provide survival and proliferative signals to the leukemic clone within lymphoid organs.

We have previously reported that T cells from low-risk CLL patients show a lower migratory capacity towards CXCL12 a chemokine produced in lymphoid organs by stromal cells or NLCs compared to T cells from high-risk patients.

Given that CXCL12 also exerts a co-stimulatory activity on T cells, we asked whether this capacity could be impaired in T cells from low-risk compared to high-risk patients favoring the indolent course of the disease in the former group.

Our results suggest that the presence of CXCL12 in lymphoid organs may enhance the activation of T cells. Because no differences were found in the co-stimulation induced by CXCL12 in T cells from both groups of CLL patients, other processes, such as the lower migratory response of low-risk T CLL cells might favor the indolent clinical course of the disease in these patients.

RS usually develops in lymph nodes and its cutaneous spread is very rare. It remains to be determined whether the expression or functionality of CCR4 is augmented in leukemic cells of CLL patients who develop other skin manifestations.

Historically, the pro-inflammatory effect of the amine was associated to its action on H1 receptors; however the use of antagonists for this receptor showed to be ineffective in the treatment of allergic diseases.

In recent years, it was assigned an important role in these pathologies to H4R, which is not clear yet. For this purpose, we use a known murine model of OVA-induced airway inflammation.

PBS: 0. PBS: In conclusion, thioperamide acting on DC could offer an alternative therapy in the treatment of allergy through the induction of a tolerogenic profile Laboratory findings suggest that N-Im Np is a syndrome mediated by the action of pro-inflammatory cytokines and chemokines CK.

The diagnosis is clinical and the presence of autoantibodies is an unusual finding. Methods: Serum samples were collected from 67 patients with Polyarticular JIA and 35 controls, 15 with other autoimmune diseases 9 with Systemic lupus erythematosus, 6 with autoimmune hepatitis and 20 from age-matched healthy controls.

Anti-CCP-positivity was correlated positively with the disease characteristics. The median age was 14 and 12 years old respectively.

Twelve patients were positive for both autoantibodies. We will evaluate a-CCP as a prognostic factor of more severe evolution of the disease.

Target cells of this infection are CD4 lymphocytes, which decrease as viral replication occurs and opportunistic diseases appear cytomegalovirus CMV infection among them.

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Como Uds. Todos estos hechos positivos para la ciencia argentina requieren indefectiblemente ser sostenidos en el tiempo.

Una sociedad integrada por sujetos que buscan respuestas a interrogantes planteados por los medios de prensa o incluso por la publicidad de diversos productos.

Es por ello, que priorizamos las exposiciones cortas sobre las conferencias, tanto de expositores extranjeros como nacionales. Bienvenidos y muchas gracias por participar de este Congreso.

As you are well aware, for several years our country for different reasons that include political persecutions, lack of economical support to perform scientific research and even to maintain a decent life standard and for few personal reasons, has suffered a constant emigration of scientist searching for a better future abroad.

However, during the past few years and due to the new policies implemented by the government the tendency of emigration is reverting.

Actually, is quite positive to verify that qualified human resources remain in the country whereas several more are trying to return back.

It is also interesting to see that argentine scientists permanently settled abroad are trying to contact and collaborate with their conational in the homeland.

The present meeting is, perhaps an accurate example of the last point mentioned. By the initiative of Dr. Piaggio, who lives in France, and with the kind help of several generous Argentine and French researchers, they decided to start a meeting to explore future collaborations between Argentine and French immunologists.

This initiative was rapidly and very welcome by both scientific communities. The main organizations to support this proposal were the French embassy and for the Argentinean counterpart the ministries of Science and Technology, Education and Health.

The active participation of this ministries remarks the on going scientific policy of the Government in order to improve both working and personal situations of the researchers, also promoting the scientific development and continuously implementing the repatriation of researchers.

All this present accomplishments for the Argentinean Scientific community must be sustained in future. The increase in the training of scientific human resources, must be go along with not only the recycling of existing research buildings and laboratories, but with also the construction of new research facilities in order to accommodate both settled researchers and those coming back after training abroad.

Scientific infrastructure in building new laboratories and scientific training of human resources must run together.

The financing of grant 13 proposal must continue and must be expanded with increased amounts to cope with changing international economic situation taking in mind that several research equipments and products are important.

Grant proposal evaluation should be improved with the possibility of reconsideration and more annual callings for grant applications will be of great benefit.

Science financing should mainly from Government budget and no from international lending institutions that conditioned the purchases, and because in the long run becomes in debt.

Salaries of all the personal involved in the scientific task should increase in close relation with the local living costs. The availability of national and international fellowships, the incorporation of new career researchers and technicians into the different Research Councils and Universities should be steady sustained, expanded and even encouraged.

This last point may avoid differences among researchers. Besides, the transference between the public and the private sector should be improved but never have to be free of a reasonable economical fee.

On the other hand, private companies should change making genuine and sustainable economic inversions also in basic research.

There are positive and negative issues that the Argentine Society of Immunology should face.

The boost of the Society is evident counting the number of presentations to the present meeting, by the increasing number of affiliations and many sponsors for this event.

However, I believe, that SAI lacks a structure to face the coming times and to confront new challenges. Our people are searching for answers on issues raised by the public media or the publicity.

I ask myself if SAI, as institution, should not take a more proactive role, organizing not only scientific meeting but also being a kind of referent to be permanent consulted I also wonder if within the SAI, we should not overcome the gap between basic and clinical research, to foster a more comprehensive knowledge.

I also wonder if the SAI should not assume a greater social commitment. It is also clear that to make this happen will require a deep change in the structure of the SAI, with greater involvement of partners, with the formation of various committees such as a teaching committee and a committee of media, among others.

The programme of this Congress was set up in order to promote collaborations among researchers. This is why we prioritize a lot of short exposures rather than conferences.

More than 40 foreign guests will participate in this Congress. It is my desire and the organizers of the event that this Congress will be the starting point of collaboration between research groups in France and Argentina, not only in projects but in the exchange of human resources.

Today, the creation of a French-Argentine Center of Immunology, seems to be utopian, but could get to take shape, only with the support of the public and private sector.

I also want my appreciation to my family who I have subtracted too many hours due to this work. Welcome and thank you very much for participating in this Congress.

This is the first time that a joint FrancoArgentine Immunology meeting has been organized. France and Argentina are two countries with major interest in basic and applied immunology.

We hope that this congress will reinforce scientific exchange and initiate new solid and long-lasting collaborations in immunology between the 2 countries so as to increase international visibility of the FrancoArgentine Immunology Network: 14 at the academic level: several collaborations have already been initiated and we hope that several others will be inspired by these three days of meetings.

We hope that everybody will appreciate this meeting in Buenos Aires and we hope that this event will be the first of a long series of fruitful scientific exchanges between the two countries.

Wellcoming words E. Since then we have continuously worked in order to reach other groups using this methodology for diagnosis or research.

On this occasion, by means of the Pre-Conference Course of the SAI, our objective is to present an update on methodology and analysis software through an outstanding group of speakers from Argentina and abroad.

It is our wish that all the topics dealt with in this event will help enhance your learning experience and background in the immunology field.

We have used 2-photon dynamic imaging to analyze T cells and DCs in intact lymph nodes and tumors ex vivo or intravitally.

We showed that stable T cell-DC interactions correlate with the induction of effective immunity, while the induction of tolerance involves brief, unstable contacts.

The adhesion molecule ICAM-1 plays a central role in this process. We also analyzed the modes of tumor invasion by cytotoxic T cells, and, more recently, the mechanisms of inhibition of anti tumor immune responses by regulatory T cells.

Together these results showed that the control of the dynamics of T cell-DC interactions plays a critical role in the outcome of T cell-mediated immune responses.

Monoclonal antibodies to CD3 promote immune tolerance. This strategy has been the matter of extensive experimental studies in models of autoimmunity such as autoimmune insulin-dependent diabetes.

Data from our laboratory were the first to show that in non obese diabetic NOD mice CD3-specific antibodies could reverse recent onset disease by restoring tolerance to beta-cell antigens.

Thus, in NOD mice presenting full-blown diabetes, a five consecutive day treatment with low doses of CD3-specific antibody induced complete and durable disease remission in absence of insulin treatment.

Recently, these results were successfully transferred to the clinic in patients presenting new onset autoimmune diabetes.

The present challenge is first, to build on these results to set the use of CD3-specific monoclonal antibodies as an established therapy in well-selected subsets of patients presenting with established autoimmunity and second, to extend their use to the organ transplantation field, where they were first introduced, taking benefit of their unique tolerance-promoting capacities.

Results will be discussed in the context of autoimmune diseases in which antibodies play a pathognomonic role. Breakdown of self-tolerance: Autoimmune Orchitis 16 Vanesa A.

Facultad de Medicina. Universidad de Buenos Aires. Spermatogenesis represents challenges to the immune system, as male gametes appear long after the establishment of immune tolerance mechanisms.

Disruption of the immune privileged status of the testis following trauma, tumor, or autoimmune orchitis often results in male infertility.

DC maturation state is a control point for the induction of peripheral tolerance or autoimmunity. Investigation of EAO will help to understand the intricate interplay among tolerance mechanisms and autoimmunity.

Animal models of CNS autoimmunity: what have we learned? The cause of MS is still mostly unknown.

Demyelination in the central nervous system in MS is thought to be mainly mediated by T helper 1 cells, although this dogma is currently heavily re discussed since recent evidence suggests an active pathogenic role of CD8 T cells in MS, which recapitulates earlier suggestions that virus may have pathogenic role in MS.

Currently the unraveling of immune-mediated pathogenesis in MS relies mostly on animal models. So far there is not one animal model that reflects all aspects seen in MS, but still the many different models are very suitable for targeting specific aspects of this disease.

By using rodent models we pinpointed several cellular and molecular pathways of potential relevance for human inflammatory diseases of the central nervous system.

The lessons learned from these models will be discussed. The full extent of differences and similarities between iTreg and nTreg cells is the subject of this presentation.

We speculate that iTreg cell development is driven by the need to maintain a non-inflammatory environment in the gut, to suppress immune responses to environmental and food allergens, and to decrease chronic inflammation, whereas nTreg cells prevent autoimmunity and raise the activation threshold for all immune responses.

Rosenzweig 17 Infectious Diseases Susceptibility Unit. However, a small number of patients develop serious, life-threatening hepatitis.

To understand reasons for this great variability in disease severity, we examined 30 Argentinean patients with HAV-induced acute liver failure in a case-controlled, cross-sectional, observational study.

In addition, we propose a pathophysiological molecular mechanism by which NKT cells mediate the liver injury that develops with HAV infection, a mechanism that may be related to one that protects against asthma and allergy.

We report a new molecular mechanism of disease in patients with Xlinked EDA-ID caused by mutations that affect the poly-ubiquitin binding of NEMO rather than its production and folding.

We found a novel mutation in exon 3 of TNFRSF6, in two patients from a consanguineous family, presented in homozygous state. This mutation changes a cytosine for a tyrosine C91Y in one of the conservative domain of the extracellular region, cysteine rich domain 2 CRD2.

Interestingly, this particular change was found in three other patients from three unrelated families, in heterozygous state.

All these SNPs are highly polymorphic and we found the ancestral allele in all of them except for c. These data strongly suggest that the C91Y mutated allele originated from a single founder.

We applied a modified likelihood-based method to estimate the age of the most recent common ancestor carrying mutation C91Y.

Extent of haplotype sharing and variability of microsatellite alleles in C91Y chromosomes suggest that this mutation arose approximately years ago.

Taking into account that GTATCC haplotype was not found in our control group nor in a previous report on Caucausian subjects from USA, we have undertaken a large study on Native American Argentinean populations, to test if the unique haplotype carrying this novel mutation is restricted to a particular ethnic group.

For instance, the SNP c. Invasive pneumococcal disease leads to significant morbidity and mortality all over the world.

Immunization with pneumococcal polysaccharide 23 valent vaccine is useful to evaluate antibody response to polysaccharide antigen in children over 2 years of age.

At present we evaluate polysaccharide response by measuring antiboby against 10 pneumoccocal specific serotypes 1, 3, 5, 6B, 7F, 9V, 14, 18C, 19F, 23F.

Pneumococcal conjugate vaccine with protein carrier, has been useful to protect children younger than 2 years of age.

Given the massive use of 7 valent conjugate vaccine, which produces a humoral immune response different from PLS vaccine, it is difficult to assess specific polysaccharide response in children who have received both vaccines.

The aim of this study is to evaluate the usefulness of an extended panel of 12 specific serotypes, 6 of which are present in polysaccharide vaccine 1, 3, 5, 7F, 11A y 33F and the other 6 are present in both vaccines 6B, 9V, 14, 18C, 19F, 23F , in children older than 2 years, who have received 23 valent and 7 valent conjugate pneumococcal vaccines.

Buenos Aires. Argentina; 3Dept. Melanoma and severe opportunistic infections, mainly fungal infections, are rare in healthy pediatric individuals.

Here, we present a case of a 13 year old male, second son from non-consanguineous parents with clinical background of atopy and upper airway infections.

At the age of 12, the patient presented a melanoma in the right 19 ear, which was successfully treated by surgery.

One year later he developed a lobar pneumonia due to Cryptococcus neoformans detected in a lung biopsy, accompanied by stools with blood.

Thus, the patient was subjected to additional immunological studies, which ruled out the occurrence of classical cellular and humoral primary and secondary immunodeficiencies.

Thus, the NK cell compartment was further investigated, assuming that an impaired NK cell function could lead to a weakened immune surveillance and the development of the observed clinical symptoms.

NK cells of this patient, although normal in number, contain an unexpectedly high percentage of CD56bright cells Classically they are characterized by susceptibility to infections.

However, autoimmune manifestations, essentially autoimmune cytopenias anemia, thrombocytopenia and neutropenia , can also be observed in PIDs as a consequence of either defective central selection or defective peripheral self-tolerance.

Defect of peripheral tolerance can be observed in the context of impaired natural Tregs nTregs development or functions.

Recently, we described three patients presenting with a severe IPEX-like syndrome starting in childhood and susceptibility to severe CMV infections.

We identified inherited mutations of the IL2Ra gene. Activated T cells were devoid of CD25 expression. Finally, we also observed a complete nTregs deficiency in patients presenting with a profound calcium influx deficiency leading to a paradoxical presentation of severe combined immunodeficiency and autoimmune manifestations.

Altogether these observations highlight the central role of nTregs in the maintenance of self-tolerance and may provide mechanistic explanations in more common autoimmune diseases.

Primary complement deficiencies PCD are rare diseases that appear at any age with severe infections, autoimmunity, angioedema or asymptomatic.

They are probably vastly under diagnosed within clinical practice. In order to improve this situation, we developed a systematic study selecting patients according with preset inclusion criteria.

The diagnostic strategy includes functional complement assays for classical and alternative pathways and C3 and C4 quantification as first step and then measure of factors according prior results.

Sixteen patients were the index case but 6 appeared after family search. We notice the beginning of symptoms at early age with a delay at the first consult and diagnose.

It must be suspected a PCD in any patient with severe or recurrent infections by capsulated bacteria, with normal quantitative and functional antibody response, atypical autoimmune disease or recurrent non allergic angioedema.

An appropriated algorithm to study the suspected cases let identify the deficit, and propose the adequate therapy. Garrahan During the past 15 years, the elucidation of the genetic etiology of an increasing number of primary immunodeficiencies allowed the application of mutation analysis as an integral part of the complete evaluation of these patients.

But a stepwise screening approach always ensures efficient and thorough evaluation of mechanisms of immune dysfunction that may underlie clinical presentation with narrowing diagnostic options, before using the molecular studies that may be required to arrive at specific diagnoses.

Firstly, not all of the patients with identical clinical and laboratory findings have mutations in the same gene, we must consider family history and additional screening tools to distinguish between several candidate disease genes before sequencing them.

In addition, we must be able to interpret when a mutation we found is actually a disease causing or a highly prevalent low penetrance mutation or even a single nucleotide private polymorphism.

Furthermore, genomic DNA sequencing, the standard approach used to characterize a possible gene mutation has certain limitations, and alternative follow-up approaches may be necessary to establish the molecular basis of the primary immunodeficiency in a given patient.

Case studies being illustrative of identification and resolution of these situations aiming to avoid misdiagnosis will be discussed.

Adriana T. Larregina Department of Dermatology, University of Pittsburgh School of Medicine Recurrent skin inflammatory diseases relay on the synchronized interaction of the immune and nervous systems which takes place during the process known as neuroinflammation.

Contact hypersensitivity, CHS and atopic dermatitis AD are prototype recurrent skin inflammatory diseases initiated and sustained by type-1 and type-2 biased T cell responses, respectively.

This inflammatory microenvironment of is initiated and controlled, at least in part, by neuropeptides. In the present lecture I will discuss the role and mechanisms employed by these two cutaneous pro-inflammatory neuropeptides regarding the regulation of skin chronic inflammatory diseases.

Breast milk immune complexes are potent inducers of oral tolerance in neonates and prevent asthma development Nicolas Glaichenhaus University of Nice-Sophia Antipolis, Valbonne, France Allergic asthma is a chronic lung disease resulting from an inappropriate T helper Th -2 responses to environmental antigens.

Early tolerance induction is an attractive approach for primary prevention of asthma. We have found that breastfeeding by antigen-sensitized mothers exposed to antigen aerosols during lactation induced a robust and long-lasting antigen-specific protection from asthma.

Protection was more profound and persistent than the one induced by antigen-exposed non-sensitized mothers. The induction of oral tolerance by milk immune complexes did not require the presence of transforming growth factor-beta in milk in contrast to tolerance induced by milk-borne free antigen.

Furthermore, 21 neither the presence of IgA in milk nor the expression of the inhibitory Fc-gamma-RIIb in the newborn was required for tolerance induction.

This study provides new insights on the mechanisms of tolerance induction in neonates and highlights that IgG immune complexes found in breast milk are potent inducers of oral tolerance.

Neutrophils, however, have, upon activation, considerable potential to cause collateral damage and harm host tissues, in particular through the release of numerous proteases such as neutrophil elastase NE , cathepsin G, proteinase-3, metalloproteases, cysteine proteases It seems therefore important for the host to protect itself by producing antiproteases.

Our presentation will present some of the most recent data in that field. Recent evidences suggest that their function is not solely restricted to chemotaxis, but also participate in many other immune functions such as dendritic cell maturation and T cell activation and differentiation.

CCL18 is a chemokine expressed in lung and lymph nodes, has an unknown receptor, is produced by antigen-presenting cells and is up-regulated by Th2 cytokines.

Conversely, this property was lost in allergic subjects in association with a decreased binding of CCL18 to its putative receptor.

Buenos Aires, Argentina Biofilms are microbial communities enclosed in a polymeric matrix adherent to inert or living surfaces.

Compelling data indicate that biofilms are structurally and dynamically complex biological systems that are crucial in the pathogenesis of many clinically important bacterial infections.

Neutrophil are essential immune effectors in the first line of defense against bacterial infections. In previous studies we determined that immobilized-eDNA also activates neutrophils.

Our new findings, based on experiments performed with P. Biofilms formed by a P. Assays with biofilms formed with mucoid P.

We conclude that eDNA immersed in the matrix of bacterial biofilms is a major proinflammatory component of P. Osteoarticular Brucellosis: inflammation, matrix metalloproteinases and induction of osteoclastogensis.

Brucella can infect and survive within human osteoblasts and this infection elicits the secretion of chemokines IL-8 and MCP-1, attractants for neutrophils and monocytes, respectively that might be involved in the osteoarticular manifestations of brucellosis.

The recruitment of phagocytes may enhance the immune response since these cells can be activated within the infection focus to secrete additional inflammatory mediators.

In particular, macrophages in inflamed tissues can differentiate not only to osteoclasts the only cells known so far to be able to degrade bone , but they also appear to accelerate bone resorption through the production of proinflammatory cytokines and matrix metalloproteinases.

On the other hand, monocytes in inflamed tissues can also accelerate bone resorption by differentiate to osteoclast, in a way that involved, B.

These results suggest that proinflammatory responses elicited by B. Alberto L. The number of host genes involved in the implementation of adaptive immunity and in the execution of constitutive and inducible innate defensive mechanisms against viruses is vast.

Likewise, pathogenic viruses have evolved many different self-protective mechanisms that operate to mask their presence within the organism and to disrupt the host defences.

The outcome of this struggle is that the hosts will generally prevail at the level of the whole organism, thus resulting in host survival, while lytic viruses will win the intracellular battle, thus warranting virus survival and spread.

The ability to counteract host responses is, however, a feature of wild-type viruses only. Viral vectors are artificial entities that have been developed to deliver therapeutic transgenes and, therefore, the transduced cells should be preserved alive.

Towards this end some viral genes are often inactivated, resulting in a breakdown of the vector ability to survive in the infected cells.

The vector genome will consequently be silenced or eliminated, which constitutes a major hurdle hampering the use of vectors in gene therapy.

This talk will summarize current evidence underlying these concepts, using HSV-1 as model, and will speculate on possible ways to counteract the host defences, allowing stable and safe transgene expression.

As most pathogens infect mammals by respiratory, digestive, urogenital tracts, these specialized barriers are thus essential sites for anti-microbial immunity.

The innate immune response to bacterial flagellin, a molecular pattern specifically expressed in mucosa, is mediated by TLR5, which is expressed on various sentinels like epithelial or dendritic cells.

The presentation will focus on mucosal immunes responses induced by the TLR5 signalisation by two experimental models: 1 a systemic administration mimicking pathogen invasion in mucosal tissues and 2 a local administration mimicking microbial colonization of mucosa.

We will present data demonstrating that sentinel cells and effectors mechanisms are different in these models.

Persistent viruses including human immunodeficiency virus HIV , hepatitis B virus HBV and hepatitis C virus HCV infect more than millions people globally causing severe clinical symptoms and high mortality.

Because human persistent viruses are heavily host-restricted in most part to humans and non-human primates , we used lymphocytic choriomeningitis virus LCMV infection of its natural host, the mouse, as a model system to study the interactions between the immune system and the pathogen during in vivo chronic viral infection.

We have uncovered unique cytokine profiles throughout the course of the infection and evaluated their biological effects at the molecular, cellular and whole organism level.

Our data support the overall conclusion that the host immune system is dysregulated or re-educated to coexist with the persistent virus and provide new insights into the parameters governing the conditioned immune responses during chronic viral infections.

Thus, activated specific T lymphocytes display a crucial role in the immune response of the host to the pathogen.

Actually, it was demonstrated that IL produced by CD4 T cells would be required to eliminate primary Mtb infection and to establish an effective memory response.

In this regard, we have demonstrated that tuberculosis patients display higher number of Treg cells compared to healthy donors.

Furthermore, patients with active disease produce higher levels of IL than healthy controls. These cells produce large amounts of IL-9 in response to the pathogen.

Thus, during active tuberculosis, Tregs, Th1, Th17 and Th9 cells would be required by the human host to fight Mtb.

Influence of Mycobacterium tuberculosis genotypes on the host immune response. Maria del C. Sasiain Academia Nacional de Medicina, Buenos Aires, Argentina 24 The influence of strain variation on the outcome of infection and on the immune response induced by Mycobacterium tuberculosis is a nascent area of research.

Unlike many bacterial pathogens, gene exchange is rare in M. Our research projects are focused on the ability of the most prevalent strains causing sensible or multidrug-resistance MDR tuberculosis in Argentina.

We are working on the innate and the adaptive immune response developed by these strains in latent infected and in tuberculosis patients.

In general, Haarlem strains are lesser immunogenic than LAM strains. Hence, it should be considered the dependency on M.

Understanding the interactions of the bacilli with the host immune system could help to develop specific and more efficient treatments.

Dendritic cells DCs are thought to play a major role in initiation of immune responses to intracellular pathogens, in part through their production of the important pro inflammatory cytokine IL In the case of infection with the intracellular protozoan T.

The ability of the tumour microenvironment to alert the innate immune system has been a long lasting question and debate.

Plasmacytoid pre-dendritic cells pDCs have a special position in linking innate and adaptive immunity. They are dedicated to the production of type I IFNs after the recognition of viral and microbial products.

TLRindependent activation of pDCs may be involved in conditions of sterile inflammation. Our results show that cytokines can act as tumour-derived endogenous danger signals that alert the immune system through they effect on pDCs.

Cancer immunosurveillance appears to be an important host protection process that inhibits carcinogenesis and maintains regular cellular homeostasis.

Cancer would develop in the rare occasion when tumor cells escape that immune response. This quite old and widely accepted paradigm has surprisingly resisted the accumulation of contradictory evidences, like i the understanding of the molecular mechanisms of carcinogenesis that makes impossible that we constantly generate cancer cells or i the fact that long-term immunocompromised patients do not have increased incidence of non-viral induced cancers.

There is an immunosurveillance of cancer, but one that depends on the memory status of the players.

In the normal setting, cancer immunosurveillance is mediated by regulatory T cells that protect rather than eliminate cancer cells; in a pre-immunized setting, cancer immunosurveillance is mediated by memory effector T cells that eradicate tumor cells.

This explains another old paradigm of cancer immunology, that preventive immunization is much more effective than therapeutic immunization.

These results have significant therapeutic implications and notably should prompt to reconsider preventive vaccination against cancer.

The microenvironment of human tumors differs, from patient to patient in their lymphocytic infiltration.

In addition, lymphocytes are not randomly scattered within the tumor but appear organized in the center of the tumor, its invasive margin and in tertiary lymphoid follicles adjacent to the tumor nests.

We have particularly analyzed large cohorts of colorectal and lung cancers and shown that the infiltration of memory T cells, with a Th1 and cytotoxic orientation, both in the center and the invasive margin of the primary tumors is a major prognostic factor since it controls tumor recurrence, probably through an immune control of potential metastatic cells.

These data allow to draw an integrated picture of how an immune reaction develops in the tumor microenvironment to control cancer spread and recurrence.

Universidad Nacional de Cordoba, Argentina. Toll-like receptors TLRs recognize molecules derived from pathogens as well as endogenous danger signals possessing similar chemical structures.

Administration of their ligands to activate antigen presenting cells has always been considered a valuable tool to promote anticancer immunity.

Interestingly, the presence of functional TLRs in cancer cells has been demonstrated, raising the question about the role that these TLRs could be playing in tumors.

We have reported that B16 murine melanoma cells as well as other tumor cell lines stimulated in vitro with a TLR4-ligand during 48h prior to their inoculation into TLR4 deficient mice TLR4lps-del , induce tumors significantly smaller than controls.

A transitory halt of tumor growth was observed in TLR4 26 deficient animals which were intratumorally treated with LPS, indicating that TLR4 present on tumor cells could positively contribute to tumor growth control.

The apoptosis-proliferation balance of LPS-stimulated B16 cells is not modified and inhibition of tumor growth was not observed in nude mice; thus we hypothesized that TLR4 triggering on B16 cells themselves could induce the expression of pro inflammatory mediators, that even if they are transitory, could dramatically alter the function of dendritic cells DCs present at the site of inoculation and switch the type of immune response elicited against the tumor.

Transcriptional analysis as well as cytokines secreted show that TLR4 triggering on B16 cells induces changes in important DCs modulators.

Our results open up new avenues for understanding the role of TLR4 in tumor cells and for identifying potential new therapy strategies for cancer.

High-risk human papillomaviruses HPV are the main etiological agent of cervical cancer, the leading cause of cancer death among women in low-income countries.

Furthermore, they are also highly associated with the development of others anogenital and oropharyngeal carcinomas. Commercially available prophylactic HPV vaccines were shown to be ineffective on pre-existing neoplastic processes, thus having no immediate impact on the actual incidence of HPV-related cancers.

HPV E7 and E6 early oncoproteins represent ideals targets for immunotherapeutic intervention due to their key role in cellular transformation and constitutive expression in HPV-associated tumors.

Recently, we have developed a recombinant E7-based vaccine, exhibiting strong immunotherapeutic properties in a well established HPV tumour model.

Vaccination of female mice with low doses of the recombinant HPV E7vaccine totally prevented tumour outgrowth, even after a 3 months rechallenge.

Therapeutic treatment of tumour-bearing mice with the vaccine-type molecule also shows a remarkable activity, completely reverting the tumor growth.

These proof-of-principle experiments demonstrate the potential applicability of our vaccine candidate to the treatment of HPV-related neoplastic lesions.

Michel Braun Institute for Medical Immunology. However, this approach has fallen short of expectations, because T cells chronically stimulated by persistent antigen often become functionally exhausted and thus do not respond appropriately to therapeutic vaccination.

On the contrary, in transplantation, immunosuppression of acute rejection is known to induce chronic pathologies in the allograft, and controlling the activity of chronicallystimulated alloreactive T cells is one major problem currently facing immunologists.

Therefore, understanding the biology of T cells chronically stimulated by persistent antigens is essential to the development of therapeutic strategies that could control many immunological disorders.

We have studied a mouse model where persistent stimulation of CD4 T cells led to multi-organ T cell infiltration.

Exposure to systemic antigen, however, deeply modified T cell function and chronically stimulated T cells developed a long-lasting state of unresponsiveness, or immune adaptation, characterised by their inability to mediate organ immune damages in vivo.

However, analysis of the gene expression profile of adapted CD4 T cells revealed the specific co-expression of genes known to promote differentiation and function of Th1 effector cells as well as genes coding for proteins that control T cell activity.

Our work aims at the identification of the molecular mechanisms responsible for the phenomenon of T cell immune adaptation to persistent antigen.

These cells account for a durable Tcell reconstitution, generating a diverse TCR repertoire and robust response to infections.

Renal transplantation may be affected by immediate injury during post-transplantation period as a result of immunological and non-immunological causes.

The two most important determinants of non-immunological injury are ischemic and reperfusion injury and brain death.

Both lead to delayed allograft function, acute rejection, and diminished graft survival in the long term consequently increasing transplant costs.

Better antibody detection tests have been developed and, as a result, hyperacute rejection is now extremely rare. In addition, different options as induction therapies have improved acute rejection rates during the first year after transplantation.

Allograft long term survival rates have not improved significantly. The development of anti- HLA antibodies, especially class II, is the main cause of transplant glomerulopathy.

This entity causes allograft chronic dysfunction. Rabinovich, Juan M. Ilarregui, Diego O. Croci, Mariana Salatino, Marta A. Toscano, Victoria Sundblad, L.

Mascanfroni, Juan P. Recent efforts toward decoding the glycosylation signature of immune cell processes have revealed dramatic changes during T cell differentiation.

These alterations are also detected during the course of dendritic cell maturation, suggesting that protein-glycan interactions may have a decisive role in the control of immune cell responsiveness and tolerance.

Blockade of galectin-1 expression results in heightened T-cell-mediated tumor rejection. Moreover, galectindeficient mice exhibit augmented TH1 and TH responses and are considerably more susceptible to immune-mediated fetal rejection and autoimmune disease than their wild-type counterparts.

Yet, the mechanistic bases underlying these anti-inflammatory effects are still uncertain. We will discuss the identification of a circuit linking galectin-1 signaling, generation of tolerogenic dendritic cells and expansion of regulatory T cells which contributes to the resolution of autoimmune inflammation and modulates T cell responses in antigen-specific and neoplastic settings.

Finally, we will highlight the role of these lattices in linking tumor hypoxia to neovascularization. As in peripheral organs, multiple TLRs are dynamically expressed appear to play important roles in both tissue surveying and repair, and are involved in mounting a host-defense response against microbial invasions.

The immune and inflammatory response that follows can either benefit the host or further contribute to pathology.

This study explores the effect of TLR agonists on the CNS and uses New World arenavirus Tacaribe, a neurotropic pathogen that is lethal in newborn mice, to explore the role of TLR-mediated innate immune responses in disease pathogenesis and treatment.

Our studies demonstrate that the TLR immune activation pathway is required for the pathogenesis of Tacaribe.

Protection was mediated by an increase in antigen-specific antibodies IgG and IgM and required inducible nitric synthase iNOS expression and nitric oxide NO production.

Biological Chemistry Dept. The pathogenic mechanisms of disease are presently unknown and the active involvement of epithelial acinar cells producing inflammatory mediators in the induction and perpetuation of the inflammatory response supports its characterization as an autoimmune exocrinopathy.

The hypothesis of an impaired balance of neuroimmune interactions in the target organ at the onset of the disease can be approached in the non-obese diabetic NOD mouse model of SS.

At the pre-diabetic stage, NOD mice have the unique characteristic of developing a deep secretory loss with mild infiltration of the glands consistent with a structural-dysfunctional aetiology.

In keeping with a defect in salivary gland homeostasis as initial trigger of the autoimmune exocrinopathy, an enhanced apoptosis of acinar cells and reduced salivary secretion and signaling upon vasoactive intestinal peptide VIP stimulation was observed.

VIP is a neuro- and immunopeptide that promotes exocrine secretion, contributes to vasodilation in exocrine glands and induces anti-inflammatory effects through its action on macrophages.

On this basis, we are currently exploring the role of apoptotic secretory epithelium as a pro-inflammatory triggering factor of exocrine dysfunction in the NOD model of Sjogren's syndrome and the modulatory effect of VIP on the dialogue of acinar cells and macrophages.

T1AD is multifactorial in origin with both genetically and environmental determinants conferring susceptibility to disease onset. Agents that fulfill these qualities have potential for therapeutic use, and might induce tolerance in autoimmune diabetes and islet transplantation.

We have recently described strong experimental evidence of the employment of galectin-1, a soluble lectin, able to restore immune balance in T1AD mouse models by means of different mechanisms.

Following a similar rationale we are now searching for novel compounds and combinatorial therapies without unacceptable risks associated with continuous immune suppression to control the autoimmune burden of T1AD and hopefully, reaching permanent arrest of autoimmunity.

DNA recognition by antibodies is at the center of autoimmune disease, in particular, in Lupus Systemic Erythemoatosus SLE , where 9 out of 10 patients are females and no specific treatment is available.

Although suspected, there is no clear proof that DNA is the actual immunogen is DNA, however, the pathogenic antibodies that cause tissue damage recognize DNA and are in fact a hallmark for the disease.

Our lab has been investigating the molecular basis for antibody-DNA recognition. We had obtained high affinity sub-nanomolar and specific monoclonal antibodies.

We present an integrated mechanistic analysis, combining structure, thermodynamics and kinetics.

Our model system is the only antibody-nucleic acid recognition out of a handful which: i antibodies were elicited by a specific a known DNA immunogen and ii have an integrated mechanism dissected with fold higher affinity.

These studies should open the posibility of combining basic research of a well described model with clinical research, comparing binding behaviour with sera antibodies from patients, and possible diagnostic applications.

More importantly, even considering that SLE is known to arise from a complex combination of genetic, environmental and other factors, our studies may constitute the basis for drug screening and design of therapeutic compounds that can block pathogenic anti-DNA autoimmune antibodies.

School of Medicine. Catholic University of Cordoba. Giardia lamblia is a human intestinal pathogen. Recently, we found that the mechanism controlling variant-specific surface protein VSP switching in Giardia involves components of the RNA interference machinery, and that disruption of this pathway generate trophozoites expressing simultaneously many VSPs.

Here, we utilize these altered trophozoites to determine the role of antigenic variation in an animal model of giardiasis.

Our results show that either primary infection with trophozoites expressing all VSPs, or immunization with purified VSPs from the transgenic cells, protects animals from subsequent Giardia infections.

These results constitute the first experimental evidence that antigenic variation is essential for parasite survival within hosts and that artificial disruption of this mechanism might be useful in generating vaccines against important pathogens that exhibit similar behaviour.

Facultad de Medicina, UBA. Argentina 31 It has been almost 30 years since the detection of the first HIV-1 cases and yet an effective and safe vaccine has not been developed.

One of the challenges to address and ultimately overcome when developing a vaccine is the high variability of HIV Studies performed in our laboratory analyzed the impact of the immunogenicity of BF recombinant variants in the design of future vaccines employing Nef and Env proteins as a model.

After prime-boost immunizations we found that a cellular response of high specificity with low cross-reactivity against subtype B was generated.

We analyzed the peptides involved in the specific and cross-reactive responses, as well as potential immunization strategies to cover the immunogenic epitopes targeted after the single B and BF immunizations.

These results will be pivotal for our region, indicating that antigens from BF viral variants must be considered for a future vaccine.

Cargnelutti1,2; M. Lacoste1,2 ; G. Rabinovich3,4 ; M. Yersiniosis is a zoonotic foodborne associated with a risk ReA. It belongs to the group of arthritidies known as the spondyloarthropathies SpA.

The pathogenesis of ReA is incompletely understood. Accordingly, IL levels were increased in synovial fluids of SpA compared with control osteoarthritis patients.

Cazorla, Fernanda M. Frank, Marina N. Matos, Carolina Ramirez, Emilio L. Several vaccines against Chagas disease have been studied; however, all vaccination regimens tested so far conferred partial immunity.

Despite the strong immune response elicited by vaccination, the parasite survival suggests that, similarly to what happens in natural infection, the immune response is either insufficient or inherently inadequate.

The major cystein proteinase, cruzipain Cz , has a catalytic domain and a C-terminal extension. Although the role of the later domain is unknown, is the major immunogenic part in infected humans.

Immunization employing full-length rCz or its N- and C-terminal domains demonstrated that the C-terminal domain allows Cz to circumvent the immune response to the catalytic N-terminal.

This is a property of the molecule itself, since inoculation of rCz produces a similar effect than Cz in natural or experimental infection.

Cz is not the only T. In addition, we demonstrated that by immunizing with the N-terminal domain alone, it is possible to differentially orient the host immune response providing a better protection than that elicited by full-length Cz.

This observation has an important implication in terms of optimizing a rational vaccine design. The parasite expresses trans-sialidase, an enzyme that transfers sialyl residues among glycoconjugates and sialylates the surface components.

The enzyme is also shed to the bloodstream. Sialyl residues incorporate strong negative charges to the glycoconjugates and are involved in several biological functions.

Therefore, the trans-sialidase-induced alterations of sialylation patterns are associated with several abnormalities observed during the infection.

In fact, the strong thymocyte depletion and the absence of germinal centers in secondary organs, together with thrombocytopenia are prevented by the passive transfer of a trans-sialidase-neutralizing mAb to infected animals.

Incorporation of the sialyl residue leads CD4CD8 thymocytes to enter apoptosis, whereas its removal induces thrombocytopenia.

A major obstacle to understand these events was the difficulty to identify the transferred residues among all those naturally occurring.

This limitation was abrogated by an unnatural sugars approach, because trans-sialidase efficiently hydrolyzed and transferred azido-sialic acids to lymphocyte surface where CD45 and integrins were identified as acceptors.

Then, trans-sialidase provides both a suitable target for chemotherapy and a tool to explore the glycobiology of the immune system. The liver was the most affected tissue with numerous cellular infiltrates, apoptotic cells and necrotic areas.

Infection increased transaminase activities in both mouse strains, although they were highest in B6 mice.

To gain insight into the molecular basis, we investigated the TLRs commitment in hepatic tissue. We found a different modulation of TLR2, 4 and 9 in this tissue, associated with an intensified proinflammatory cytokine profile in B6.

Notably, Pam3CSK4 TLR2-agonist treatment, previous to infection, induced a significant reduction of transaminase levels and inflammatory foci in liver of B6 mice.

Proinflammatory cytokines were decreased and TGFb increased by B6 purified hepatic leukocytes. Our results describe some of danger signals involved in liver response and clearly demonstrate that Pam3CSk4, previous to infection, can attenuate the exacerbated hepatic inflammation.

After the invasion process, trypomastigotes are temporally contained in a membrane vesicle known as the parasitophorous vacuole TcPV.

Subsequently the parasites escape to the cytoplasm and differentiate into amastigotes replicating actively.

Host cell invasion is governed by trypomastigotes-triggered activation of host cell signaling pathways. At least two main invasion process have been described: the calciumdependent recruitment and fusion of lysosomes with the host plasma membrane, and the activation of a class I PI 3-kinases that leads to the invagination of the plasma membrane generating a vacuole initially devoid of lysosomal markers.

Work from our laboratory indicates that the TcPV is decorated by the autophagic protein LC3 33 and that that autolysosomes are recruited to T.

Interestingly, activation of autophagy before infection significantly increased the number of infected cells whereas inhibitors of this pathway reduced invasion.

In addition, the absence of critical proteins required for autophagosome formation, limited parasite entry. These results indicate that mammalian autophagy is a key process that favors the internalization of T.

We observed that expression of FOXP3 in activated PBMCs was already present above baseline before any cell division, indicating that was induced in cells that were previously negative for this transcription factor.

Finally, those conditions in which iTregs may play a central role can be associated with the expansion of Tregs observed in the pre-implantation phase of the menstrual cycle and during pregnancy.

Intriguingly, in contrast to many cell types, skeletal muscle fibers do not physiologically express detectable levels of major histocompatibility class I MHC -I molecules.

This model revealed that tolerance to muscle autoantigens implies ignorance for CD4 and, presumably, peripheral deletion for CD8 T cells.

In contrast to other autoimmune models based on tissue-specific expression of a neo-autoantigen, transfer of anti-Ova T cells to SM-Ova mice did not lead to myositis while Ova-bearing tumors were rejected, presumably because of lack of muscle MHC-I expression.

It was known that induction of muscle H-2Kb expression in iMHC Tg mice provokes a severe myopathy, seemingly through the presentation of cryptic muscle autoantigens to autoreactive T cells.

Proteomic analysis evidenced up-regulation of chaperonins and UPR proteins characteristic of endoplasmic reticulum stress.

Hence, expression of H-2Kb by muscle fibers may be pathogenic per se. Many host-reactive T-cells were identified but they were anergized in these human chimeras.

Responses in vitro and in vitro antibody production, cytotoxic activity against virus-infected target cells were extremely effective despite the lack of HLA molecule shared between T-cells and all other cells of the body.

The differentiation of stem cells into mature Tcells in the context of a foreign host thymus therefore led to the selection of T-cell recognition structures of a peculiar type.

Morelli T. Starzl Transplantation Institute. University of Pittsburgh, Pittsburgh, PA. During the past decade, there has been a shift from the perception of dendritic cells DCs solely as professionalantigen Ag -presenting cells APCs capable of inducing immunity to the view that these cells are also crucial regulators of tolerance.

Most of the current DC-based methods to induce donor-specific immunosuppression for transplantation rely on the passive transfer of in vitro-generated DCs rendered immature, maturation-resistant MR- or alternatively-activated by pharmacological or genetic manipulation.

However, this simple idea has not been tested in vivo. The effect on the anti-donor response was independent of the method used to generate therapeutic DCs or their viability, and in accordance with the idea that recipient APCs mediate the effects of therapeutic DCs in transplantation, prolongation of allograft survival was achieved using donor apoptotic MR-DCs or those lacking surface MHC molecules.

In conclusion, our findings indicate that DC-based therapies modulate the anti-donor response through recipient APCs and that the systemically injected immunosuppressive DCs function as Ag-transporting cells rather than APCs to prolong allograft survival.

Comparing efficacy in larger animal models is yet to be performed, and our study does not preclude future generation of immunosuppressive DCs capable of directly mediating T cell suppression.

But given the cost, time and risk of DC-based therapies, our data raise some concern on the potential benefits of current DC-based therapies in transplantation over previously tested and simpler methods like donor-specific transfusion.

Universidad de la Republica. Montevideo, Uruguay. Different parameters are critical to engineer tolerogenic dendritic cells Tol-DCs to be used as therapeutic tools to manipulate antigen-specific immune responses.

Injection of autologous Tol-DC same strain than the recipient is able to prolong allograft survival significantly. Although the reasons of this difference have not been established, autologous Tol-DC imply practical advantages to be used in a clinical setting.

When autologous TolDCs not pulsed with donor antigens are associated to sub-optimal immunosuppression, a synergistic effect is 35 achieved, leading to donor-specific allograft tolerance.

We will discuss the immunological mechanisms of this effect and the advantage to use autologous tolerogenic dendritic cell therapy in organ transplantation.

We will treat the reasons why this is a clinically relevant approach and the experimental data that support this strategy.

The Tn Ag is expressed on human carcinoma-associated mucin variant and has attracted increasing interest in clinical oncology since it is widely expressed in a variety of adenocarcinomas.

Intradermal immunization with MAG:Tn3 induced high levels of Th2 cytokines and anti-Tn antibodies recognizing human tumor cells.

This meeting was possible thanks to the Argentine and French Immunological Society, especially to Dr. Eduardo Chuluyan and all the professionals that have been invited to this important Congress.

Daniela Di Giovanni, who worked hard with me to make this event possible. Since we have began a hard and long struggle against many obstacles we found in the way in the every day routine; making diagnosis and treatments for patients with immunodeficiency diseases.

In the last ten years the development of the Clinical Immunology let us get better diagnoses and treatments and good evolution in our patients.

We could make a question to ourselves: Why? What kind of the Immunology do we really want? What kind of medicine do we want? This is a fundamental question that most of us are asking?

Does it make sense to participate in the existing world order? We want a world where life is preserved, and the quality of life is enriched for everybody, not only for the privileged.

But our way is very long, there are lots of thing to do and we feel very lonely in this battle, because we receive little help from our government and some private laboratories.

In Argentina small group of professional and foundations are doing what they can do with a few tools but with passion.

Passion lives here. Heart is what drives us and determines our fate. I would like for the people who works with health, people who ask questions, who bend the rules and take risks, people like all of you in this room.

In our country a young group of doctors, biochemical and Parents Society are working together to spread all the information they get about IDP.

More than Highly dynamic interactions of phagosomes, first with endosomes and then with lysosomes, lead to the maturation of phagosomes into phagolysosomes.

Contrary to others phagocytes, which degrade ingested particles to amino acids, dendritic cells only partially degrade ingested proteins, preserving protein fragments that associate to MHC molecules for the onset of adaptative immune responses.

To do so, dendritic cells have developed a specialized phagocytic system, different from that of other phagocytes, such as macrophages or neutrophiles.

In contrast to other phagocytes, which acidify their phagosomes very actively, dendritic cells maintain a neutral or slightly alkaline pH in phagosomes.

In addition, dendritic cells phagosomes present several other unique functional specializations, including the capacity to export phagocytosed molecules to the cytosol or to recruit ER resident proteins.

In order to further understand the role of these phagocytic specializations in cross presentation, we have analyzed the molecular mechanisms involved.

Using shRNAmediated knock-down of different proteins, we have evaluated the role of ER-recruitment to phagosomes in cross presentation.

Our studies show that dendritic cells have developed a specialized phagocytic pathway, highly adapted to their main function, the presentation of phagocytosed antigens for the initiation and the control of adaptative immune responses.

This metabolic pathway is responsible for reactive oxygen species generation during respiratory burst, then associated to germ killing within phagocytic cells, and inflammatory reactions.

CGD patients typically suffer from two types of clinical manifestations: recurrent bacterial and fungal infections, and dysregulated granulomata formation.

Early diagnosis, antimicrobial prophylaxis, and aggressive management of infectious complications are the cornerstones of CGD management.

These three measures have strikingly improved life expectancy and quality of life in the last fifty years.

Interestingly, very encouraging and promising results have been lately achieved with definitive and curative options for this disease.

Besides, new aspects regarding genetic pathophysiology, genotype-phenotype correlation, microbiological susceptibility, and new potential therapeutic approaches will also be discussed.

Antibodies associated to autoimmune disease and B cell compartment in pediatric patients with Chronic Granulomatous Disease. The recurrent infections are the result of this 37 defect.

Also are observed abnormally exuberant inflammatory responses leading to granuloma formation such as granulomatous enteritis, genitourinary obstruction.

In 10 CGD patients pts ,mean age: 11 years, range: 3 X-linked -gp91phox, 5 autosomal recessive 4 p47phox; 1 p67phox and 2 with no molecular diagnosis, half of them with some gastrointestinal involvement, we evaluated the prevalence of different antibodies associated to autoimmune diseases and characterize peripheral B cell compartment and correlate with clinical features of CGD.

We found high prevalence of ASCA in our CGD pts as has been reported in inflammatory bowel disease, but do not know what the real clinical value in these pts.

Most our CGD had B cell compartments defects with normal functional antibody response. In our follow-up on that the defect in B cells is only phenotypic.

It would be interesting to evaluate regulatory pathways that control B cell differentiation, which could be implicated in this phenomenon.

We describe unrelated patients with mycobacterial disease and a dominantnegative IRF8 allele. Autosomal dominant IRF8 deficiency is therefore a novel genetic etiology of mycobacterial disease.

Despite Mendelian inheritance in most cases, mutations of a given gene can lead to a variable expression of the corresponding disease.

Somatic mutations can be a key event in this process, either by reverting a profound inherited defect or by strengthening a partial deficiency.

Reversion mutations were described in numerous cases and restored the impaired expression or function of a gene product, thereby leading to an attenuated clinical phenotype.

In most cases, ALPS is the consequence of germline mutations with partial clinical penetrance. We now found in families carrying mutations 38 with low clinical penetrance that combined germline and somatic mutations of the FAS gene could account for the onset of ALPS in patients, whereas carriers of only the germline mutation remained asymptomatic.

This observation illuminates the impact of somatic mutations in the expression of ALPS and may have further implications in the phenotypical variability of some primary immunodeficiencies or in the onset of other autoimmune diseases.

The national registry did not distinguish data between from different centers and we did not have more processed information than it was published.

While we are registering all immunodeficient patients again, we still do not have any processed information from it.

So we have to show the analyzed data of our group as recorded by ouerselves. From the creation of the Group in until , we had primary immunodeficient patients.

Since our group has had out of these were classified according to the IUIS classification. We think that the great increase in the number of patients with immunological diagnosis in the last three years is mainly due to more than one cause.

Finally, we emphasize the importance of an Argentinean registry for the Argentinean patients. Three Centers experience: A model for patient care in pediatric immunology in Rosario Dr.

Within this net, the ICP unit, carries out different activities which involve professional training and lecturing.

During January June , patients were diagnosed with PID as follows: antibody deficiencies Others: familial haemophagocityc lymphohistiocytosis 3 patients and citophagic histiocytic panniculitis 1 patient.

Bringing the ICP unit into the Health Care System has allowed an early detection and derivation of patients suspected of having some kind of immunological disorder, it has also allowed a more efficient use of existing health care resources and an adequate use of other services.

Our goal was to know the incidence and prevalence of primary immunodeficiencies PIDs and their frequency. The PDI represents a low percentage of the general pathology and the information obtained in the registry increases the chances for early diagnosis and treatment and reduces morbidity and mortality.

One Center recording in La Plata Dra. In the last years the hospital has produced 14 discharges per year. The creation of the Immunology Unit dates from and consists of an outpatient, a day hospital care and a hospitalization area.

There is also a bone marrow transplant unit as part of the Hematology Service. Since there have been registered patients with primary immunodeficiency PID.

The distribution is the following: patients with antibody deficiencies Other PID diagnosed were 5 patients with granulocyte defects 1.

The remaining patients are diagnosed with: familial lymphohistiocytosis 0. Although there is a correlation with international registrations, we have a slight underreporting in SCID probably due to the severity and early death in these children.

Bruton recognized that an eight-year-old child with a four-year history of many serious septic episodes was incapable of making significant quantities of immunoglobulin.

The first congenital agammaglobulinemic patient was diagnosed. After that many primary immunodeficiencies PID have been described.

Recurrent bacterial infection is the hallmark of humoral primary immunodeficiencies PID. These patients suffer from life-threatening infections, and the goal standard of their treatment is the prevention of infections.

The need for immunoglobulin Ig replacement therapy was and still remains the mainstay of therapy not only for humoral PID but for some combined T and B-cell immunodeficiencies and for many others PID.

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