Pharmazentrum Frankfurt / ZAFES, Goethe University Hospital, Frankfurt am Main, Germany.
Curr Opin Rheumatol. 2012 Jul;24(4):417-23. doi: 10.1097/BOR.0b013e3283533719.
It is the current opinion that pathogens, such as viruses, are contributing to the development of type 1 diabetes (T1D) in susceptible individuals. This opinion is based on epidemiological associations, direct isolation of pathogens from the islets of Langerhans, as well as a large amount of data from various experimental animal models. Human enteroviruses have dominated the literature associated with the etiology of T1D. However, virus infections have also been reported to protect from autoimmune disorders.
Here we review the evidence for virus infections to be involved in the pathogenesis of T1D and discuss potential mechanisms of how such infections could accelerate the destruction of insulin-producing β-cells. In addition, we will review evidence from epidemiologic and experimental animal studies showing that virus infections could also have protective properties.
Virus infections play an important role in the pathogenesis of T1D by inducing or accelerating the autodestructive process, but also by protecting from autoimmunity. Thus, multiple sequential infections might shape the autoreactive immune repertoire and the pathogenesis of T1D in a complex fashion.
目的综述:目前认为,病原体(如病毒)在易感个体中促成了 1 型糖尿病(T1D)的发生。这种观点是基于流行病学关联、从胰岛直接分离病原体,以及大量来自各种实验动物模型的数据。人类肠道病毒在与 T1D 病因学相关的文献中占据主导地位。然而,也有报道称病毒感染可预防自身免疫性疾病。
最新发现:本文综述了病毒感染参与 T1D 发病机制的证据,并讨论了此类感染如何加速破坏胰岛素产生β细胞的潜在机制。此外,我们还将回顾来自流行病学和实验动物研究的证据,表明病毒感染也可能具有保护作用。
总结:病毒感染通过诱导或加速自身破坏性过程在 T1D 的发病机制中发挥重要作用,但也可通过预防自身免疫来发挥作用。因此,多次序贯感染可能以复杂的方式塑造自身反应性免疫库和 T1D 的发病机制。