Dysfunction of regulatory T cells in pathogenesis of type 1 diabetes mellitus

Type 1 diabetes (T1D) is an autoimmune disease characterized by insulin deficiency. Abnormal autoimmunity targeting the pancreatic islets leads to dysfunction of pancreatic cells and the inability to secrete insulin. The pathogenesis of abnormal autoimmunity in T1D is complex. Currently, it is widely believed that regulatory T cells (T ) are involved in the process of the onset of T1D. T primarily maintain immune tolerance by suppressing effector T cell (T ) by direct contact or by the release of cytokines. Numerous studies have shown defects in the immunosuppressive function of T in autoimmune diseases, such as T1D. Compared with healthy individuals, T1D patients exhibit abnormalities in the frequency, function, gene expression, apoptosis, related signaling pathways, and cytokines of T . This review summarizes how deficiencies in T in the aforementioned aspects are involved in the pathogenesis of T1D and helps to develop novel treatment methods by understanding the underlying mechanisms of action.