Swanson-Mungerson Michelle, Longnecker Richard
Department of Microbiology and Immunology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.
Trends Immunol. 2007 May;28(5):213-8. doi: 10.1016/j.it.2007.03.002. Epub 2007 Mar 29.
Epstein-Barr virus (EBV) has been associated with autoimmune diseases for over 40 years. However, the mechanisms by which EBV might promote autoimmune development remain elusive. Many of the hypotheses for the means by which EBV might achieve this incorporate the idea that autoimmune responses are initially immune responses against EBV proteins that crossreact with endogenous human proteins. However, recent evidence using transgenic mouse models suggests that B cells expressing the EBV-encoded protein latent membrane protein 2A (LMP2A) bypasses normal tolerance checkpoints and enhances the development of autoimmune diseases. Evidence from transgenic mouse models supports a paradigm in which LMP2A could promote autoimmune development. This novel model provides a framework to test potential mechanisms by which EBV could promote the development of autoimmune responses and might enable the identification of strategies to treat EBV-associated autoimmune diseases.
四十多年来，爱泼斯坦-巴尔病毒（EBV）一直与自身免疫性疾病有关。然而，EBV促进自身免疫发展的机制仍不清楚。关于EBV实现这一目标的方式，许多假设都包含这样一种观点，即自身免疫反应最初是针对与内源性人类蛋白质发生交叉反应的EBV蛋白的免疫反应。然而，最近使用转基因小鼠模型的证据表明，表达EBV编码蛋白潜伏膜蛋白2A（LMP2A）的B细胞绕过了正常的耐受性检查点，促进了自身免疫性疾病的发展。转基因小鼠模型的证据支持了一种LMP2A可促进自身免疫发展的模式。这个新模型提供了一个框架，用于测试EBV促进自身免疫反应发展可能的机制，并可能有助于确定治疗EBV相关自身免疫性疾病的策略。
