Viruses and Type 1 diabetes: a dynamic labile equilibrium.

Darius A Schneider, Matthias G von Herrath
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Abstract

Type 1 diabetes (T1D) results from the specific immune-mediated destruction of the insulin-producing β-cells of the pancreas. In genetically susceptible individuals, a still undetermined initiating 'hit' triggers a cascade of events that eventually leads to autoreactive CD8 T cells infiltrating the pancreatic islets and, subsequently, destroying them. There is increasing evidence that viruses, especially enteroviruses, are major environmental candidates; however, despite decades of investigation, we still lack certainty with regard to the causation of T1D. Moreover, studies in animal models of diabetes suggest a protective role of certain enteroviral infections upon diabetes contraction, making the quest for viral involvement in T1D even more difficult. Analyzing the foundation and the results of the most current work in the field, this article gives a brief overview of current knowledge, as well as providing an outlook for future directions.

病毒与 1 型糖尿病:一种动态的易变平衡。
1 型糖尿病(T1D)是由于胰腺中产生胰岛素的 β 细胞受到特异性免疫介导的破坏所致。在遗传易感人群中,一个仍未确定的起始 "打击 "引发了一连串事件,最终导致自体反应性 CD8 T 细胞浸润胰岛,进而破坏胰岛。越来越多的证据表明,病毒(尤其是肠道病毒)是主要的环境候选者;然而,尽管进行了几十年的调查,我们仍然无法确定 T1D 的病因。此外,对糖尿病动物模型的研究表明,某些肠道病毒感染对糖尿病的罹患具有保护作用,这使得寻找病毒与 T1D 的关系变得更加困难。本文分析了该领域最新研究的基础和结果,简要概述了当前的知识,并对未来的研究方向进行了展望。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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