实用肝脏病杂志 ›› 2014, Vol. 17 ›› Issue (6): 665-669.doi: 10.3969/j.issn.1672-5069.2014.06.029

• 综述 • 上一篇    下一篇

Toll样受体在肝衰竭发病中的作用研究进展*

薛源综述, 韩悦, 张欣欣审校   

  1. 200025 上海市 上海交通大学医学院附属瑞金医院感染病科
  • 收稿日期:2014-02-10 出版日期:2014-12-31 发布日期:2016-04-11
  • 通讯作者: 张欣欣,E-mail: zhangxinxinrj@163.com
  • 作者简介:薛源,男,30岁,博士研究生,主治医师。主要从事病毒性肝炎的临床和实验研究。E-mail: xueyuan80908@163.com
  • 基金资助:
    国家973项目十二五重大科技专项(2012ZX10002007)

Toll-like receptors in pathogenesis of liver failure

Xue Yuan, Han Yue, Zhang Xinxin   

  1. Department of Infectious Diseases, Ruijin Hospital Affiliated to Medicine School of Shanghai Jiaotong University,Shanghai 200025, China
  • Received:2014-02-10 Online:2014-12-31 Published:2016-04-11

摘要: 肝衰竭是多种病因引起的肝功能失代偿,其发病机制涉及肝细胞的坏死、凋亡、再生、肝脏纤维化等。Toll样受体(TLR)作为一种模式识别受体,参与了固有免疫反应和获得性免疫反应,在肝衰竭的发病中起重要作用。动物实验和临床研究均已证实TLR与肝细胞的坏死有关。脂多糖(LPS)、D-氨基半乳糖(D-GalN)、刀豆素A(ConA)、CpG寡脱氧核苷酸(CpG ODN)、多聚肌苷酸-多聚胞苷酸(Poly I:C)和对乙酰氨基酚(APAP)所致的肝损伤需要不同的TLR通路参与。TLR3、TLR4、TLR9参与了肝细胞的凋亡。TLR7对肝纤维化有保护作用。TLR基因多态性研究可以从宿主方面揭示肝衰竭的发病机制,为个体化诊疗提供依据。

关键词: 肝衰竭, Toll样受体, 凋亡

Abstract: Liver failure caused by many etiologies,is a deficiency of liver. Its pathogenesis still remains unclear, and it might involve necrosis,apoptosis and regeneration of the hepatocytes,and fibrosis of the liver. As a kind of pattern recognition receptor,Toll-like receptors(TLRs) link the innate and adaptive immune response,and play an important role in the pathogenesis of liver failure. Animal experiments and clinical studies have demonstrated that TLRs are related to the necrosis of liver cells. Liver injury which is caused by different agents,such as LPS,D-GalN, ConA,CpG ONA,Poly(I:C)and APAP,needs different TLRs signaling. TLR3,TLR4 and TLR9 signaling can promote apoptosis of liver cells. TLR7 signaling has a protective effect against liver fibrosis. Research on TLR polymorphism can reveal the pathogenesis of liver failure from the host aspect, and provide evidences for individualized diagnosis and treatment of patients with liver failure.

Key words: Liver failure, Toll like receptor, Apoptosis