β-Cell autophagy in the pathogenesis of type 1 diabetes

Type 1 diabetes is an insulin-dependent, autoimmune disease where the pancreatic beta cells are destroyed resulting in hyperglycemia. This multifactorial disease involves multiple environmental and genetic factors, and has no clear etiology. Accumulating evidence suggests that early signaling defects within the beta cells may promote a change in the local immune milieu leading to autoimmunity. Therefore, many studies have been focused on intrinsic beta-cell mechanisms that aid in the restoration of cellular homeostasis under environmental conditions that cause dysfunction. One of these intrinsic mechanisms to promote homeostasis is autophagy, defects which are clearly linked with beta-cell dysfunction in the context of type 2 diabetes. Recent studies have now also pointed towards beta-cell autophagy defects in the context of type 1 diabetes. In this perspectives review, we will discuss the evidence supporting a role for beta-cell autophagy in the pathogenesis of type 1 diabetes, including a potential role for unconventional secretion of autophagosomes/lysosomes in the changing dialogue between the beta cell and immune cells.

Automated summary

Type 1 diabetes is an insulin-dependent autoimmune disease characterized by destruction of pancreatic beta cells leading to hyperglycemia. Research suggests that defects in autophagy may be linked with beta-cell dysfunction in type 1 diabetes, sparking investigations into the role of this mechanism in disease pathogenesis.