Department of Medicine, Mount Sinai School of Medicine, Immunology Institute, 1425 Madison Avenue, New York, NY 10029, USA.
Immunol Res. 2012 Dec;54(1-3):50-68. doi: 10.1007/s12026-012-8311-9.
Genetic composition and major histocompatibility complex polymorphisms unequivocally predispose to autoimmune disease, but environmental factors also play a critical role in precipitating disease in susceptible individuals. Notorious among these has been microbial infection. Older studies describing associations between microbial infection and autoimmune disease are now followed by new studies demonstrating correlations between susceptibility to autoimmune disease and commensal colonization of the intestinal tract. T helper 17 (T(H)17) cells have gained a prominent role in autoimmune disease, and notably, their development within the intestine has been linked to colonization with specific commensal bacteria. Here, we consider current views on how microbes, T(H)17 cells, and autoimmunity are connected. We speculate on how the intricate relationships among commensal, pathogen, and the host might ultimately determine susceptibility to autoimmune disease.
遗传组成和主要组织相容性复合体多态性明确导致自身免疫性疾病，但环境因素在易患个体中引发疾病方面也起着关键作用。其中臭名昭著的是微生物感染。描述微生物感染与自身免疫性疾病之间关联的旧研究现在被新的研究所跟进，这些研究证明了自身免疫性疾病易感性与肠道共生定植之间的相关性。辅助性 T 细胞 17（T(H)17）细胞在自身免疫性疾病中扮演着重要角色，值得注意的是，它们在肠道内的发育与特定共生细菌的定植有关。在这里，我们考虑了目前关于微生物、T(H)17 细胞和自身免疫之间联系的观点。我们推测共生体、病原体和宿主之间错综复杂的关系如何最终决定自身免疫性疾病的易感性。
