MOLECULAR MIMICRY - A MECHANISM FOR AUTOIMMUNE INJURY
MOLECULAR MIMICRY - A MECHANISM FOR AUTOIMMUNE INJURY
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DOI：
10.1096/fasebj.6.3.1740233
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发表时间：
1992-02-01
期刊：
影响因子：
4.8
通讯作者：
FUJINAMI, RS
中科院分区：
文献类型：
--
作者：
BARNETT, LA;FUJINAMI, RS
许多机制可以解释病毒感染后免疫介导的病理学。虽然已经假设了几种方式在疾病中发挥作用，但病毒诱导的自身免疫的一种广泛接受的机制是分子模拟。据认为，这种损害可能是由于对病毒和宿主之间共享的类似区域的免疫反应造成的。利用计算机辅助分析，已经鉴定出病毒和宿主抗原之间的许多序列同源性。在某些情况下，针对这些区域的肽的单克隆抗体已经显示出在动物模型中直接诱导或增强疾病。使用这种方法来鉴定相似的区域，有可能将已知的自身抗原与自身免疫性疾病中的感染因子相关联，其中没有已知的病原体。相反，也可能将已知的病毒成分与未知的宿主抗原相关联。此外，鉴定自身抗原或病毒蛋白的疾病诱导区域可能导致免疫学方法来建立对这些疾病诱导区域的耐受性或无反应性。
Many mechanisms may account for immune-mediated pathology after viral infections. Although several means have been hypothesized to play a role in disease, a widely accepted mechanism for viral-induced autoimmunity is molecular mimicry. It is thought that damage could result from an immune response to similar regions shared between virus and the host. Using computer-aided analysis, many sequence homologies have been identified between virus and host antigens. Using peptides corresponding to these regions, immunologic cross-reactivity has been found. In some cases, monoclonal antibodies to peptides of these regions have been shown to directly induce or augment disease in animal models. Using this approach to identify similar regions, it is possible to associate a known autoantigen with an infectious agent in autoimmune diseases in which there is no known etiologic agent. Conversely, it would also be possible to associate a known viral constituent with an unknown host antigen. Furthermore, identification of disease-inducing regions of autoantigens or viral proteins may lead to immunotherapeutic approaches to establish tolerance or anergy to such disease-inducing regions.