Mannering S I, Pathiraja V, Kay T W H
Immunology and Diabetes Unit, St Vincent's Institute of Medical Research.
Department of Medicine, St Vincent's Hospital, University of Melbourne, Fitzroy, VIC, Australia.
Clin Exp Immunol. 2016 Jan;183(1):8-15. doi: 10.1111/cei.12699. Epub 2015 Oct 21.
Type 1 diabetes (T1D) develops when there are insufficient insulin-producing beta cells to maintain glucose homeostasis. The prevailing view has been that T1D is caused by immune-mediated destruction of the pancreatic beta cells. However, several recent papers have challenged the long-standing paradigm describing T1D as a tissue-specific autoimmune disease. These authors have highlighted the gaps in our knowledge and understanding of the aetiology of T1D in humans. Here we review the evidence and argue the case for the autoimmune basis of human T1D. In particular, recent analysis of human islet-infiltrating T cells brings important new evidence to this question. Further data in support of the autoimmune basis of T1D from many fields, including genetics, experimental therapies and immunology, is discussed. Finally, we highlight some of the persistent questions relating to the pathogenesis of human type 1 diabetes that remain to be answered.
1型糖尿病（T1D）在产生胰岛素的β细胞不足以维持葡萄糖稳态时发生。主流观点认为，T1D是由免疫介导的胰腺β细胞破坏所致。然而，最近的几篇论文对将T1D描述为组织特异性自身免疫性疾病的长期范式提出了挑战。这些作者强调了我们在人类T1D病因学知识和理解方面的差距。在此，我们回顾相关证据，并论证人类T1D自身免疫基础的情况。特别是，最近对人类胰岛浸润性T细胞的分析为这个问题带来了重要的新证据。还讨论了来自遗传学、实验疗法和免疫学等许多领域的支持T1D自身免疫基础的进一步数据。最后，我们强调了一些与人类1型糖尿病发病机制相关的仍有待解答的持续性问题。
