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 regs)
are involved in the process of the onset of T1D. T regs
primarily maintain immune tolerance by suppressing effector T cell (T
eff) by direct contact or by the release of cytokines.
Numerous studies have shown defects in the immunosuppressive function of
T regs 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 regs. This review
summarizes how deficiencies in T regs 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.