Type 1 diabetes (T1D) is an autoimmune disease in which an inappropriate self-directed immune response affects and destroys insulin-producing Beta-cells in pancreatic islets leading to dysregulated blood glucose levels. T1D may affect people of any age, its clinical presentation is highly variable, and its incidence is increasing worldwide (1). The initial triggering events of T1D are unknown and their elucidation is of pivotal importance. Several factors might lead to the breakdown of Beta-cell-specific T-cell tolerance, including genetics, exogenous infectious pathogen, noninfectious environment agents, endogenous superantigens, or physiological stress events (2).
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