摘要
肝脏中大量的巨噬细胞、自然杀伤细胞(natural killer,NK)、自然杀伤T细胞(natural killer Tcell,NKT)等构成了天然免疫系统。这一系统细胞功能紊乱,发生Th-1极化,使促炎症因子产生增多,促进了非酒精性脂肪性肝炎(nonalcoholic steatohepati-tis,NASH)的形成;肝脏持续的暴露于这些炎症因子,可以促进多种促纤维化因子产生,但Th-2细胞因子分泌的不足,使NASH进一步发展为肝硬化的现象却相对比较少见。本文就肝脏天然免疫系统在非酒精性脂肪肝病(nonalcoholic fatty liver disease,NAFLD)中的调节机制作一综述。
The liver is rich in macrophages （ ie, Kupffer cells）, natural killer cells, which constitute the innate immunity system. Defects in this system promoting Th-1 polarization of hepatic cytokines is co/nmon pathogenic mechanisms for nonalcoholic steatohepatitis, Although chronic inflammation induces production of various profibrogenic factors, progression to latter stages of nonalcoholic fatty liver dis- ease is relatively unusual in individuals with NASH. This may reflect that Th-2 cytokines are critical to the pathogenesis and progression of latter stages of nonalcoholic fatty liver disease. This review will focus on these developments to clarify how inflammatory mediators from the hepatic innate immunity system mediate the pathogenesis of nonalcoholic fatty liver disease.
出处
《安徽医药》
CAS
2007年第4期289-291,共3页
Anhui Medical and Pharmaceutical Journal
基金
安徽省科技公关计划项目(No06013134B)
安徽省高等学校省级自然科学研究重点项目课题(No2006KJ095A)
