Schneider Darius A, von Herrath Matthias G
Center for Type 1 Diabetes Research, 9420 Athena Circle, La Jolla, CA 92037, USA.
Diabetes Manag (Lond). 2013 May;3(3):217-223. doi: 10.2217/dmt.13.17.
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.
1型糖尿病（T1D）是由胰腺中产生胰岛素的β细胞受到特定的免疫介导破坏所致。在具有遗传易感性的个体中，一个尚未确定的起始“触发因素”引发一系列事件，最终导致自身反应性CD8 T细胞浸润胰岛并随后将其破坏。越来越多的证据表明，病毒，尤其是肠道病毒，是主要的环境候选因素；然而，尽管经过数十年的研究，我们仍不确定T1D的病因。此外，糖尿病动物模型研究表明某些肠道病毒感染对糖尿病的发生具有保护作用，这使得探寻病毒与T1D的关联变得更加困难。本文通过分析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。
