Experimental diabetes


Group Leader

Marika Falcone


Autoimmune disease results from the interplay between environmental and genetic factors. Recent studies indicated that autoimmune diseases like Type 1 Diabetes (T1D) are induced by genetic or environment-induced alterations of immune regulatory pathways whose function is to avoid or limit the activation/expansion of self-reactive T lymphocytes. The aim is to determine whether a defect of immuneregulation underlies the pathogenesis of autoimmune diabetes in mice and humans and to restore those regulatory pathways for prevention/treatment of T1D.

Research activity

Type 1 Diabetes (T1D) is an autoimmune disease mediated by self-reactive T cells that destroy insulin-producing β cells of the pancreatic islets. Both genetic and environmental factors are involved in T1D pathogenesis but the mechanisms governing the activation of islet-specific autoimmune T cells are still largely unknown. Growing evidence supports the notion that the gut environment influences the pathogenesis of extra-intestinal autoimmune diseases such as T1D. Specifically, an inflammatory intestinal environment induced by diet and/or commensal microbiota composition can promote activation of autoimmune T cells including islet-specific T cells thus affecting T1D pathogenesis. This unit demonstrated that T1D patients have alteration of gut mucosal immunity and it is currently studying in humans and animal models of T1D how gut inflammation, modification of microbiota composition and intestinal and mucus barrier integrity affect the autoimmune pathogenesis of T1D. Moreover, researchers are exploiting the capacity of probiotic and prebiotic therapeutic approaches to modulate T1D pathogenesis in pre-clinical models with the ultimate goal to design clinical trials aimed at preventing T1D in genetically “at risk” T1D children.