慢性乙肝致炎的细胞分子机制

Cellular and molecular mechanisms of liver inflammation in chronic hepatitis B

慢性乙肝是一种由HBV介导的以肝脏局部多种炎性细胞浸润的慢性感染性疾病。HBV侵入机体后能否形成慢性感染与病毒是否变异、宿主抗病毒免疫应答强弱等因素密切相关。免疫耐受、Th1/Th2失衡、HBV肝外PBMC感染等是导致乙肝持续感染迁延难愈的重要原因。机体对在清除侵入的病毒时,可对受感染的肝细胞产生一定程度损伤,如CTL通过分泌穿孔素和表达Fasl等途径诱导靶细胞凋亡;肝脏中嗜中性粒细胞和单核巨噬细胞通过产生反应氧(ROS)、一氧化氮(NO)反应氮等中间产物,介导损伤受感染的肝细胞,在局部形成以单核/巨噬细胞浸润为主炎性损伤和炎性反应。

Chronic hepatitis B,a type of chronic infectious disease,is mediated by the hepatitis B virus（HBV） and causes infiltration of inflammatory cells at multiple sites in the liver.After HBV invades the body,it can produce a chronic infection and the virus may mutate;the virus is closely associated with the level of the host＇s immune response to the virus and other factors.Immunotolerance,a Th1/Th2 imbalance,and HBV infection in PBMCs are major causes that lead to persistent liver infection and delayed healing.In order to eliminate the invading virus,some infected hepatocytes may be injured via cytotoxic T lymphocytes（CTL） that secrete perforin and express FasL.In response,neutrophilic granulocytes and mononuclear macrophages produce oxygen（ROS）,nitric oxide（NO）,and other intermediate metabolites and play key roles in hepatocyte damage and local inflammatory infiltration.