非酒精性脂肪性肝病先天免疫机制的研究进展

Research advances in innate immunity mechanism of nonalcoholic fatty liver disease

非酒精性脂肪性肝病(NAFLD)的发病机制和疾病进展与先天免疫系统的激活密切相关。综述了各类免疫细胞、Toll样受体及其下游信号通路参与胰岛素抵抗、介导氧化应激和肝脏炎症及纤维化过程。树突状细胞的减少或消除可延迟肝脏炎症反应和纤维组织增生的发生。自然杀伤T淋巴细胞的减少在单纯脂肪变阶段可诱导脂质积累,而在炎症阶段可减轻纤维化进程。胰岛素及氨基酸m TOR信号通路可通过短期或长期调控抑制自噬过程,引起内质网应激及胰岛素抵抗状态改变,从而影响NAFLD的发生发展。中医药治疗NAFLD的机制研究亦愈来愈偏向免疫机制方向。

The pathogenesis and progression of nonalcoholic fatty liver disease（ NAFLD） are closely associated with the activation of the innate immune system. This article reviews how various types of immune cells,Toll- like receptors,and their downstream signaling pathways are involved in insulin resistance and mediate oxidative stress,inflammation,and fibrosis in the liver. Reduction or elimination of dendritic cells delays inflammatory responses and fibrosis in the liver. A decrease in natural killer T cells induces lipid accumulation at the stage of simple steatosis,but alleviates fibrosis at the inflammation stage. The m TOR signaling pathways for insulin and amino acids suppresses autophagy through short- term or long- term regulation,which leads to endoplasmic reticulum stress and altered insulin resistance,thereby modulating the development and progression of NAFLD. The research on the mechanisms by which traditional Chinese medicine offers therapeutic benefits for NAFLD increasingly focuses on the potential role of immunity.