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作 者:吴胜男 孙为豪[1] WU Shengnan;SUN Weihao(Department of Geriatric Gastroenterology,the First Affiliated Hospital of Nanjing Medical University,Nanjing 210029,China)
机构地区:[1]南京医科大学第一附属医院老年消化科,江苏南京210029
出 处:《南京医科大学学报(自然科学版)》2022年第1期147-152,共6页Journal of Nanjing Medical University(Natural Sciences)
基 金:国家自然科学基金(81072030)。
摘 要:自身免疫性胃炎(autoimmune gastritis,AIG)是一组由异常自身免疫反应所介导的疾病,其发病机制复杂,目前尚未完全阐明。近年来对其发病机制有一些新认识,文章将对于该疾病的遗传易感性、免疫机制、幽门螺杆菌(Helicobactor pylori,Hp)感染等方面的研究进展进行简要归纳和阐述。AIG可能为多因素、多基因致病,遗传易感性的发现,免疫调节机制的改变,Hp感染及维生素D缺乏机制为阐明AIG的发病机制带来新的曙光。针对Fas/FasL通路的靶向性治疗,操纵Toll样受体信号,开发针对细胞因子的新疗法有望抑制炎症性疾病,根除HP及积极补充维生素D都能抑制AIG的发生发展。Autoimmune gastritis,induced by abnormal autoimmune reaction,has a complicated pathogenesis and unclarified etiologies.Recently,some new progresses have been made on the pathogenesis of autoimmune gastritis.This article briefly summarizes and describes the new advances of the pathogenesis observed in genetic susceptibility,immunemechanism,and Helicobacter pylori(Hp)infection.Autoimmune gastritis may be caused by multiple factors and genes.The discovery of genetic susceptibility,the change of immune regulation mechanism,HP infection and the lack of vitamin D bring new dawn to clarify the pathogenesis of autoimmune gastritis.Targeted therapy for Fas/FasL pathway,manipulation of Toll-like receptor signal and development of new therapies for cytokines are expected to inhibit inflammatory diseases.Eradication of HP and active supplementation of vitamin D can inhibit the occurrence and development of autoimmune gastritis.
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