Division of Gastroenterology, Department of Medicine, University of California, San Diego, School of Medicine, La Jolla, California 92093-0702, USA.
J Gastroenterol Hepatol. 2013 Aug;28 Suppl 1(0 1):38-42. doi: 10.1111/jgh.12019.
Activation of innate immune systems including Toll-like receptor (TLR) signaling is a key in chronic liver disease. Recent studies suggest that gut microflora-derived bacterial products (i.e. lipopolysaccharide [LPS], bacterial DNA) and endogenous substances (i.e. high-mobility group protein B1 [HMGB1], free fatty acids) released from damaged cells activate hepatic TLRs that contribute to the development of alcoholic (ASH) and non-alcoholic steatohepatitis (NASH) and liver fibrosis. The crucial role of TLR4, a receptor for LPS, has been implicated in the development of ASH, NASH, liver fibrosis, and hepatocellular carcinoma. However, the role of other TLRs, such as TLR2 and TLR9 in chronic liver disease remains less clear. In this review, we will discuss the role of TLR2, 4, and 9 in Kupffer cells and hepatic stellate cells in the development of ASH, NASH, and hepatocarcinogenesis.
先天免疫系统的激活，包括 Toll 样受体 (TLR) 信号通路，是慢性肝病的关键。最近的研究表明，肠道微生物群衍生的细菌产物（即脂多糖 [LPS]、细菌 DNA）和受损细胞释放的内源性物质（即高迁移率族蛋白 B1 [HMGB1]、游离脂肪酸）激活肝 TLR，导致酒精性（ASH）和非酒精性脂肪性肝炎（NASH）以及肝纤维化的发生。TLR4 是 LPS 的受体，其在 ASH、NASH、肝纤维化和肝癌的发生发展中起着关键作用。然而，其他 TLR，如 TLR2 和 TLR9 在慢性肝病中的作用尚不清楚。在这篇综述中，我们将讨论 TLR2、4 和 9 在库普弗细胞和肝星状细胞中在 ASH、NASH 和肝癌发生中的作用。
