The type 1 diabetes, autoimmune is the most common chronic diseases of childhood and adolescence, with grave prognosis if treated inadequately. There is heterogeneity in its clinical expression, depending on the extent of the destruction of pancreatic beta cells by autoreactive T lymphocytes. The presence of autoantibodies and genotype predisposing (HLA class II) allows the diagnosis of the disease. An autoimmune process relapsing-remitting type was proposed, involving the interference of viral infections in the loss of beta cells, gradually, but not linear. The spontaneous remission, "honeymoon", clinically detected around 50% of children with type 1 diabetes, it is timely to study immunological events. Focusing immunosuppression physiological extensively studied in experimental models, different populations of dendritic cells influence the onset of autoimmunity by the expansion of regulatory T cells by stimulation via IL-10, TGFß, indoleamine 2,3-dioxygenase (IDO). In vitro, IDO induces the expression of HLA-G, HLA class I molecule nonclassical in human dendritic cells, and both molecules cooperate to immunosuppression. However, there are few tools to identify cells that mediate the disease in humans. The objective of the study is to identify, in peripheral blood of patients with type 1 diabetes, the expression of HLA-G, IDO, as well as other markers of activated T cells, B and dendritic. An individual assessment at different stages of the disease will be included when possible: at diagnosis, remission and subsequent developments. The data will be associated with humoral markers.
News published in Agência FAPESP Newsletter about the scholarship: