Massilamany C, Gangaplara A, Reddy J
School of Veterinary Medicine and Biomedical Sciences, University of Nebraska-Lincoln, Lincoln, NE, USA.
Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.
Scand J Immunol. 2015 Jun;81(6):469-75. doi: 10.1111/sji.12297.
The eye generally is considered to be an immune-privileged organ, but this notion is being increasingly challenged as ocular antigens can be expressed in the generative lymphoid organs, resulting in attainment of self-tolerance. What triggers a break in this tolerant state is a fundamental question in autoimmunity research. The general belief is that exposure to environmental microbes can break self-tolerance in genetically susceptible individuals, leading to the induction of autoimmune responses. The molecular mimicry hypothesis has been proposed as one major mechanistic, pathway through which microbes, by generating cross-reactive immune responses, can induce ocular damage of the kind that might occur in uveitis. However, our recent data suggest that exposure to microbial products containing mimicry epitopes for retinal antigens can potentially be beneficial to the host. In this review, we discuss the immune mechanisms with particular reference to the molecular mimicry hypothesis as it relates to immune-mediated uveitis.
眼睛通常被认为是一个免疫赦免器官，但随着眼部抗原可在生成性淋巴器官中表达，从而实现自身耐受，这一概念正受到越来越多的挑战。触发这种耐受状态的打破是自身免疫研究中的一个基本问题。普遍认为，接触环境微生物会打破基因易感个体的自身耐受，导致自身免疫反应的诱导。分子模拟假说已被提出作为一种主要的机制途径，通过该途径，微生物通过产生交叉反应性免疫反应，可诱导葡萄膜炎中可能出现的那种眼部损伤。然而，我们最近的数据表明，接触含有视网膜抗原模拟表位的微生物产物可能对宿主有益。在这篇综述中，我们特别参照与免疫介导性葡萄膜炎相关的分子模拟假说，讨论免疫机制。
