Delogu Lucia Gemma, Deidda Silvia, Delitala Giuseppe, Manetti Roberto
Department of Drug Science, University of Sassari, Italy.
J Infect Dev Ctries. 2011 Oct 13;5(10):679-87. doi: 10.3855/jidc.2061.
Autoimmunity occurs when the immune system recognizes and attacks host tissue. In addition to genetic factors, environmental triggers (in particular viruses, bacteria and other infectious pathogens) are thought to play a major role in the development of autoimmune diseases.
We searched PubMed, Cochrane, and Scopus without time limits for relevant articles.
In this review, we (i) describe the ways in which an infectious agent can initiate or exacerbate autoimmunity; (ii) discuss the evidence linking certain infectious agents to autoimmune diseases in humans; and (iii) describe the animal models used to study the link between infection and autoimmunity.
Besides genetic predisposition to autoimmunity, viral and bacterial infections are known to be involved in the initiation and promotion of autoimmune diseases. These studies suggest that pathogens can trigger autoimmunity through molecular mimicry and their adjuvant effects during initiation of disease, and can promote autoimmune responses through bystander activation or epitope spreading via inflammation and/or superantigens.
当免疫系统识别并攻击宿主组织时，自身免疫就会发生。除了遗传因素外，环境触发因素（特别是病毒、细菌和其他传染性病原体）被认为在自身免疫性疾病的发展中起主要作用。
我们在PubMed、Cochrane和Scopus上搜索了无时间限制的相关文章。
在本综述中，我们（i）描述了感染因子引发或加剧自身免疫的方式；（ii）讨论了将某些感染因子与人类自身免疫性疾病联系起来的证据；（iii）描述了用于研究感染与自身免疫之间联系的动物模型。
除了自身免疫的遗传易感性外，已知病毒和细菌感染参与自身免疫性疾病的引发和促进。这些研究表明，病原体可通过分子模拟及其在疾病起始过程中的佐剂作用引发自身免疫，并可通过旁观者激活或经由炎症和/或超抗原的表位扩展促进自身免疫反应。
