Cooke A, Ferraccioli G F, Herrmann M, Romani L, Schulze C, Zampieri S, Doria A
Department of Pathology, University of Cambridge, Cambridge, UK.
Clin Exp Rheumatol. 2008 Jan-Feb;26(1 Suppl 48):S1-7.
It is thought that in genetically predisposed individuals, autoimmune diseases can be promoted and/or exacerbated by viruses, bacteria, or parasitic infectious agents. Pathogens can activate innate immune response interacting with Toll-like receptors that recognize pathogen-associated molecules. As a consequence of infections, a prolonged inflammatory response may occur leading to chronic inflammation with activation of adaptive immune response. In addition, the defective clearance of apoptotic infected cells, which progress- es to secondary necrosis, can foster the autoimmune reactions. Although numerous data from humans and/or animal models support the hypothesis of a direct contribution of pathogens to the induction of the disease, some infectious agents are able to prevent autoimmune disorders. In this review, data on the innate and adaptive immune response induced by pathogens are summarized, focusing on the possible protective or non-protective role of infections in the development of autoimmune diseases.
人们认为,在具有遗传易感性的个体中,自身免疫性疾病可由病毒、细菌或寄生虫感染因子引发和/或加重。病原体可激活与识别病原体相关分子的Toll样受体相互作用的固有免疫反应。感染的结果可能是发生持续的炎症反应,导致慢性炎症并激活适应性免疫反应。此外,凋亡感染细胞的清除缺陷(进展为继发性坏死)可促进自身免疫反应。尽管来自人类和/或动物模型的大量数据支持病原体直接导致疾病的假说,但一些感染因子能够预防自身免疫性疾病。在本综述中,总结了病原体诱导的固有免疫和适应性免疫反应的数据,重点关注感染在自身免疫性疾病发展中可能的保护或非保护作用。