Ercolini Anne M, Miller Stephen D
Department of Microbiology-Immunology and Interdepartmental Immunobiology Center, Feinberg School of Medicine, Northwestern University, 303 E. Chicago Avenue, Chicago, IL 60611, USA.
Neurol Res. 2005 Oct;27(7):726-33. doi: 10.1179/016164105X49508.
Although the immune system evolved to protect the host from foreign infection, it can sometimes recognize and attack host tissues, a phenomenon known as autoimmunity. In addition to genetic factors, environmental elements such as viruses and bacteria are thought to play a role in the development of autoimmune diseases. The major hypothesized mechanism by which infection with these agents can lead to autoimmunity is termed molecular mimicry. Here, immune responses initiated against foreign antigens are cross-reactive with self-antigens. This is thought to occur especially if the foreign antigen is similar in structure or amino acid sequence to the self-antigen. In this review, we explore evidence for the role of molecular mimicry in neurological diseases.
尽管免疫系统的进化是为了保护宿主免受外来感染，但它有时会识别并攻击宿主组织，这种现象被称为自身免疫。除了遗传因素外，病毒和细菌等环境因素也被认为在自身免疫性疾病的发展中起作用。这些病原体感染导致自身免疫的主要假说机制被称为分子模拟。在这里，针对外来抗原引发的免疫反应与自身抗原具有交叉反应性。人们认为，特别是当外来抗原在结构或氨基酸序列上与自身抗原相似时，就会发生这种情况。在这篇综述中，我们探讨了分子模拟在神经系统疾病中作用的证据。
