Research
Autoimmunity and Tolerance
Autoimmunity is a consequence of the breakdown of self-tolerance leading the immune system to attack organs and tissues. Autoimmune diseases have no cure until now and comprise a wide spectrum of diseases that collectively affect approximately 5 to 10% of the developed world population and are a significant cause of morbidity and mortality. The pathogenesis of autoimmune diseases involves a particular combination of genetic, immune, hormonal, and environmental factors. Although to this date some factors such as sunlight exposure affecting vitamin D levels, nutritional habits, xenobiotics, and hygiene have been associated to autoimmunity, the true cause of the breaking of the immune balance is still largely unknown. We work on trying to understand the mechanisms involved in the development of autoimmune diseases. We believe that an altered traffic and localization of antigen presenting cells such as dendritic cells and B-lymphocytes are key components in the development of these diseases.
Immune System and Cancer
T helper 17 (Th17) lymphocytes, a subset of T helper cells, first described in autoimmune disorders are characterized by the production of IL-17 and other pro-inflammatory cytokines and are though to play a role in inflammation. Interestingly, Th17 cells have been found to infiltrate several types of tumors; however, their function in tumor immunity is still unclear. Recent studies designed to understand the role of these lymphocytes in tumor progression have yielded contradictory results. Thus, depending on the methodological approach applied, Th17 appeared to possess either anti-tumor or pro-tumor properties. These conflicting results could be explained by the presence of two types of Th17 cells; “inflammatory” IFN-g-producing Th17 cells and “immunosuppressive” Th17 cells (iTh17), which produce factors that mediate tumor progression. Recently, others and we have demonstrated that Th17 cells generated with IL-6 and TGF-bexpress the CD39 and CD73 ectonucleotidases and produce adenosine. We are currently trying to dilucidate whether CD39 and CD73 ectonucleotidases are able to confer Th17 cells with an immunosuppressive function.