J Pathol. 2013 May;230(1):1-3. doi: 10.1002/path.4174. Epub 2013 Mar 12.
Type 1 diabetes (T1D) is caused by the destruction of insulin-producing pancreatic β cells by the patient's immune system. While the underlying genetics and immunopathology are fairly well characterized, the environmental trigger remains unidentified. Numerous studies have centred on the role of enteroviruses as aetiological factors that could initiate or accelerate T1D development. The most convincing evidence to date consists of an array of reports documenting the presence of enteroviral nucleic acids in peripheral blood at diagnosis. A prominent hypothesis is that enteroviruses may infect the pancreatic islets and thus be responsible for the islet-specific up-regulation of MHC class I that is commonly observed, possibly enabling T cell recognition and cytotoxicity. Past immunohistochemical studies have indeed shown that antibodies binding the enteroviral capsid protein VP1 preferentially stain the pancreatic β cells from diabetic individuals. New data now indicate that the VP1 antibody used in these studies cross-reacts with mitochondrial proteins.
1 型糖尿病（T1D）是由患者免疫系统对产生胰岛素的胰腺β细胞的破坏引起的。虽然潜在的遗传学和免疫病理学特征相当明确，但环境触发因素仍未确定。许多研究集中在肠道病毒作为可能引发或加速 T1D 发展的病因因素的作用。迄今为止最令人信服的证据是一系列报告，记录了在诊断时外周血中存在肠道病毒核酸。一个突出的假设是肠道病毒可能感染胰岛，从而导致常见的胰岛特异性 MHC Ⅰ类上调，可能使 T 细胞识别和细胞毒性。过去的免疫组织化学研究确实表明，与肠道病毒衣壳蛋白 VP1 结合的抗体优先染色来自糖尿病患者的胰腺β细胞。新的数据现在表明，这些研究中使用的 VP1 抗体与线粒体蛋白发生交叉反应。
