La Jolla Institute for Allergy and Immunology - LIAI, 9420 Athena Circle, La Jolla, CA 92037, USA.
Expert Rev Clin Immunol. 2011 Jan;7(1):45-53. doi: 10.1586/eci.10.91.
The emergence of autoreactivity that ultimately destroys insulin-producing β-cells and causes Type 1 diabetes (T1D) is a result of genetic susceptibility and environmental factors, such as viral infections. The ability to induce strong cellular immune responses and to cause inflammation in the target organ makes viral infections prime candidates for the initiation of islet autoreactivity. Indeed, certain viruses have been linked to the occurrence of T1D based on epidemiological, serological and histological findings; and several rodent studies clearly demonstrate that viral infections can trigger autoimmunity. However, viruses have also been shown to efficiently prevent autoimmunity, which underlines the beneficial aspects of exposure to microbial agents as suggested by the hygiene hypothesis. Here, we will try to untangle some aspects of the complex interplay between viruses and the immune system and we will recapitulate by what rationale certain viruses have been associated with T1D.
自身免疫反应的出现最终会破坏产生胰岛素的β细胞并导致 1 型糖尿病(T1D),这是遗传易感性和环境因素(如病毒感染)共同作用的结果。病毒具有诱导强烈细胞免疫反应和引起靶器官炎症的能力,使其成为胰岛自身免疫反应起始的主要候选者。事实上,某些病毒已根据流行病学、血清学和组织学发现与 T1D 的发生相关;并且几项啮齿动物研究清楚地表明,病毒感染可引发自身免疫。然而,病毒也被证明可以有效地预防自身免疫,这强调了暴露于微生物制剂的有益方面,正如卫生假说所建议的那样。在这里,我们将尝试理清病毒与免疫系统之间复杂相互作用的一些方面,并回顾一下为什么某些病毒与 T1D 有关。