Type 1 diabetes is an insulin-dependent, autoimmune disease where the pancreatic beta cells are destroyed resulting in hyperglycemia. This multi-factorial 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 mileu, contributing to autoimmunity. Therefore, many studies have been focused on intrinsic beta cell mechanisms that aid in restoration of cellular homeostasis under environmental conditions that cause dysfunction. One of these intrinsic mechanisms to promote homeostasis is autophagy, defects in 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.

中文翻译：

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β 细胞自噬在 1 型糖尿病发病机制中的作用

1 型糖尿病是一种胰岛素依赖的自身免疫性疾病，其中胰腺 β 细胞被破坏导致高血糖。这种多因素疾病涉及多种环境和遗传因素，病因不明。越来越多的证据表明，β 细胞内的早期信号缺陷可能会促进局部免疫环境的变化，从而导致自身免疫。因此，许多研究都集中在内在 β 细胞机制上，这些机制有助于在导致功能障碍的环境条件下恢复细胞稳态。促进体内平衡的这些内在机制之一是自噬，其缺陷与 2 型糖尿病背景下的 β 细胞功能障碍明显相关。最近的研究现在还指出了 1 型糖尿病背景下的 β 细胞自噬缺陷。