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白细胞介素-23/辅助性 T 细胞 17 轴在乙型肝炎中的关键作用。

Pivotal roles of the interleukin-23/T helper 17 cell axis in hepatitis B.

机构信息

Institute of Immunology, PLA, Third Military Medical University, Chongqing, China.

出版信息

Liver Int. 2012 Jul;32(6):894-901. doi: 10.1111/j.1478-3231.2012.02764.x. Epub 2012 Feb 19.

DOI:10.1111/j.1478-3231.2012.02764.x
PMID:22340646
Abstract

T helper 17 (Th17) cells are a newly identified subset of T helper cells that play important roles in host defense against extracellular bacteria, as well as in the pathogenesis of autoimmune disease. Research interest in these cells was piqued when hepatitis B virus (HBV)-infected patients were found to have significantly elevated Th17 cell frequency, and it was proposed that these proinflammatory effectors may promote the HBV disease process. Subsequent studies have revealed that Th17 cells drive immune-mediated pathology of HBV infection, and that IL-23 amplifies the Th17 cell responses and liver inflammation. As a result, new pathways of HBV-mediated liver damage have been elucidated, along with promising new targets of molecular therapeutic strategies. Ongoing research is also providing significant insights into the target cells and underlying mechanisms of Th17-secreted cytokines, including IL-17A, IL-21 and IL-22. Future studies are expected to fully uncover the cytokine-related mechanisms mediating HBV-induced liver inflammation, and to determine the yet unknown cell source of IL-23. This review will draw upon the most up-to-date available data to discuss the putative roles and detailed mechanisms of IL-23/Th17 cell axis in HBV infection-mediated liver pathogenesis.

摘要

辅助性 T 细胞 17(Th17)细胞是一种新鉴定的辅助性 T 细胞亚群,在宿主抵抗胞外细菌以及自身免疫性疾病发病机制中发挥重要作用。当乙型肝炎病毒(HBV)感染患者的 Th17 细胞频率显著升高时,人们对这些细胞产生了研究兴趣,并提出这些促炎效应物可能促进 HBV 疾病进程。随后的研究表明,Th17 细胞驱动 HBV 感染的免疫介导性病理,IL-23 扩增 Th17 细胞反应和肝炎症。因此,HBV 介导的肝损伤的新途径已经阐明,以及有前途的分子治疗策略的新靶点。正在进行的研究还为 Th17 分泌细胞因子(包括 IL-17A、IL-21 和 IL-22)的靶细胞和潜在机制提供了重要的见解。未来的研究有望充分揭示介导 HBV 诱导的肝炎症的细胞因子相关机制,并确定 IL-23 尚不清楚的细胞来源。本综述将利用最新的可用数据讨论 IL-23/Th17 细胞轴在 HBV 感染介导的肝发病机制中的假定作用和详细机制。

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