Restoring homeostasis of CD4+ T cells in hepatitis-B-virus-related liver fibrosis
Restoring homeostasis of CD4+ T cells in hepatitis-B-virus-related liver fibrosis
复制标题
DOI：
10.3748/wjg.v21.i38.10721
复制
发表时间：
2015-10-14
影响因子：
4.3
通讯作者：
Jiang, Wei
中科院分区：
文献类型：
--
作者：
Cheng, Li-Sha;Liu, Yun;Jiang, Wei
免疫介导的肝损伤在乙型肝炎病毒（HBV）感染过程中较为常见。HBV免疫清除失败会导致慢性肝炎，并增加肝硬化和肝细胞癌的发病风险。HBV相关肝纤维化（HBVLF）由HBV引发的慢性肝炎发展而来，是慢性乙型肝炎（CHB）与肝硬化之间的一个可逆的中间阶段。因此，明确HBVLF的发病机制对改善临床治疗效果具有重要意义。近年来，CD4(+) T细胞的稳态被认为在HBVLF进程中起着关键作用。为更深入揭示其潜在机制，在本综述中，我们系统回顾了不同CD4(+) T细胞亚群对CHB和HBVLF的影响。我们着重阐述了CD4(+) T细胞的稳态以及调节性T细胞（Treg）与辅助性T细胞17（Th17）之间的重要平衡。我们还讨论了一些与Treg和Th17细胞相关的细胞因子，如白细胞介素（IL）-17、IL - 22、IL - 21、IL - 23、IL - 10、IL - 35和IL - 33，以及程序性细胞死亡蛋白1、细胞毒性T淋巴细胞相关抗原4、含T细胞免疫球蛋白结构域和黏蛋白结构域分子3和大麻素受体2等表面分子，这些分子对CHB和HBVLF中CD4(+) T细胞的稳态具有潜在治疗意义。
Immune-mediated liver injury is widely seen during hepatitis B virus (HBV) infection. Unsuccessful immune clearance of HBV results in chronic hepatitis and increases the risk of liver cirrhosis and hepatocellular carcinoma. HBV-related liver fibrosis (HBVLF), occurring as a result of HBV-induced chronic hepatitis, is a reversible, intermediate stage of chronic hepatitis B (CHB) and liver cirrhosis. Therefore, defining the pathogenesis of HBVLF is of practical significance for achieving better clinical outcomes. Recently, the homeostasis of CD4(+) T cells was considered to be pivotal in the process of HBVLF. To better uncover the underlying mechanisms, in this review, we systematically retrospect the impacts of different CD4(+) T-cell subsets on CHB and HBVLF. We emphasize CD4(+) T-cell homeostasis and the important balance between regulatory T (Treg) and T helper 17 (Th17) cells. We discuss some cytokines associated with Treg and Th17 cells such as interleukin (IL)-17, IL-22, IL-21, IL-23, IL-10, IL-35 and IL-33, as well as surface molecules such as programmed cell death protein 1, cytotoxic T lymphocyte-associated antigen 4, T cell immunoglobulin domain and mucin domain-containing molecule 3 and cannabinoid receptor 2 that have potential therapeutic implications for the homeostasis of CD4(+) T cells in CHB and HBVLF.