Kohm Adam P, Fuller Kevin G, Miller Stephen D
Department of Microbiology-Immunology and Interdepartmental Immunobiology Center, Northwestern University Medical School, 303 E. Chicago Avenue, Chicago, IL 60611, USA.
Trends Microbiol. 2003 Mar;11(3):101-5. doi: 10.1016/s0966-842x(03)00006-4.
Although the etiology of autoimmune diseases remains largely unknown, a prevailing theory concerns the infection-induced activation of self-reactive lymphocytes via the process of molecular mimicry. Here, we discuss the theory of molecular mimicry and its continued evolution from the initial basic considerations of sequence similarity to the current theories of structural homology. Such findings serve to further our understanding of T-cell receptor degeneracy and might one day provide a direct link between infection and autoimmune disease.
尽管自身免疫性疾病的病因在很大程度上仍然未知，但一种流行的理论认为，感染通过分子模拟过程诱导自身反应性淋巴细胞的激活。在此，我们讨论分子模拟理论及其从最初对序列相似性的基本考虑到当前结构同源性理论的不断演变。这些发现有助于加深我们对T细胞受体简并性的理解，也许有一天能在感染和自身免疫性疾病之间建立直接联系。
