Münz Christian, Lünemann Jan D, Getts Meghann Teague, Miller Stephen D
Viral Immunobiology, Institute of Experimental Immunology, University Hospital Zürich, Winterthurerstrasse 190, CH-8057 Zürich, Switzerland.
Nat Rev Immunol. 2009 Apr;9(4):246-58. doi: 10.1038/nri2527.
The predisposition of individuals to several common autoimmune diseases, such as rheumatoid arthritis, systemic lupus erythematosus and multiple sclerosis, is genetically linked to certain human MHC class II molecules and other immune modulators. However, genetic predisposition is only one risk factor for the development of these diseases, and low concordance rates in monozygotic twins, as well as the geographical distribution of disease risk, suggest the involvement of environmental factors in the development of these diseases. Among these environmental factors, infections have been implicated in the onset and/or promotion of autoimmunity. In this Review, we outline the mechanisms by which viral infection can trigger autoimmune disease and describe the pathways by which infection and immune control of infectious disease might be dysregulated during autoimmunity.
个体对几种常见自身免疫性疾病(如类风湿性关节炎、系统性红斑狼疮和多发性硬化症)的易感性在基因上与某些人类MHC II类分子和其他免疫调节因子相关。然而,遗传易感性只是这些疾病发生的一个风险因素,同卵双胞胎的低一致性率以及疾病风险的地理分布表明环境因素参与了这些疾病的发生。在这些环境因素中,感染被认为与自身免疫的发生和/或发展有关。在本综述中,我们概述了病毒感染引发自身免疫性疾病的机制,并描述了在自身免疫过程中感染和传染病免疫控制可能失调的途径。