Keynote: Professor Agnes Lehuen

The physiopathology of type 1 diabetes involves deregulation of both the innate and the adaptive immune system inducing loss of self-tolerance and islet destruction. Anti-islet T cells are key effector cells in the killing of pancreatic beta cells. However beta cells also participate to their own demise by recruiting innate immune cells to the islets and participating to a critical interplay with neutrophils, which initiates local inflammation and subsequent autoimmune responses. Other innate immune cells such as the plasmacytoid dendritic cells play an ambivalent role as they can participate to islet inflammation by producing type 1 IFN as well as diabetes prevention by inducing Treg cells. Similarly to Treg cells, innate-like NKT cells exert a major role in maintaining peripheral tolerance and inhibiting the development of autoimmune diabetes. Moreover our recent data suggest that another innate-like T cell population, the mucosal-associated invariant T (MAIT) cells play a regulatory role in type 1 diabetes. Even though MAIT cells can be cytotoxic against pancreatic beta cells, they are abundant in the gut mucosa and exert a protective role by maintaining gut integrity thereby controlling the development of autoimmune responses to pancreatic beta cells.