Béland Kathie, Lapierre Pascal, Alvarez Fernando
World J Gastroenterol. 2009 Mar 7;15(9):1025-34. doi: 10.3748/wjg.15.1025.
The pathogenesis of autoimmune hepatitis (AIH) is complex. However, it is believed that a susceptible individual, owing to his genetic background, sex and age, can develop the disease following exposure to an environmental trigger. Autoimmune hepatitis does not follow a Mendelian pattern of inheritance; hence no single causative genetic locus has been identified. However, several genes, inside and outside the HLA locus, have been linked to an increased susceptibility to AIH. Epidemiological evidence also suggests that the sex and age of the patient plays a role in AIH pathogenesis as the disease onset occurs mainly in the two first decades of life and a higher disease incidence is observed in females. No environmental trigger has been identified, but several have been proposed, mainly viruses and xenobiotics. This article aims at reviewing the current knowledge on susceptibility factors leading to AIH and putative triggers, emphasizing fundamental mechanisms responsible for the break of liver immunological tolerance.
自身免疫性肝炎(AIH)的发病机制复杂。然而,人们认为,由于遗传背景、性别和年龄等因素,易感个体在接触环境触发因素后可能会患上这种疾病。自身免疫性肝炎并不遵循孟德尔遗传模式;因此,尚未确定单一的致病基因位点。然而,HLA基因座内外的几个基因已被证实与AIH易感性增加有关。流行病学证据还表明,患者的性别和年龄在AIH发病机制中起作用,因为该病主要发生在生命的头二十年,且女性的发病率更高。尚未确定环境触发因素,但已提出了几种,主要是病毒和外源性物质。本文旨在综述目前关于导致AIH的易感因素和假定触发因素的知识,强调导致肝脏免疫耐受破坏的基本机制。