Mast cells contribute to autoimmune diabetes by releasing interleukin-6 and failing to acquire a tolerogenic IL-10+ phenotype

摘要: Abstract Mast cells (MCs) are innate immune that exert positive and negative modulatory functions capable to enhance or limit the intensity and/or duration of adaptive responses. Although MCs crucial regulate T cell immunity, their action in pathogenesis autoimmune diseases is still debated. Here we demonstrate play a role T1D so selective depletion conditional MC knockout NOD mice protects them from disease. diabetic overly inflammatory secrete large amounts IL-6 favors differentiation IL-17-secreting at site autoimmunity. Moreover, while control acquire an IL-10 + phenotype upon interaction with FoxP3 + Treg cells, do not undergo this tolerogenic differentiation. Our data indicate unable contribute T1D.