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CD8+T淋巴细胞在非酒精性脂肪性肝炎中的作用
DOI: 10.12449/JCH241026
利益冲突声明：本文不存在任何利益冲突。
作者贡献声明：赵一鸣负责设计论文框架及撰写论文；李开楊负责指导撰写文章并最后定稿；杨梅负责论文修改；赵琦负责指导撰写文章。
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摘要: 非酒精性脂肪性肝炎（NASH）是一种与代谢综合征密切相关的肝脏疾病，其发病机制包括胰岛素抵抗、脂质代谢紊乱、炎症反应等方面。本文简述了CD8+T淋巴细胞通过Fas-Fas配体（FasL）信号通路、释放穿孔素和颗粒酶以及分泌肿瘤坏死因子（TNF）α等细胞因子三种途径发挥细胞毒性作用特异性杀伤病毒及肿瘤靶细胞参与免疫调节；同时总结了CD8+T淋巴细胞促进巨噬细胞招募且与自然杀伤T淋巴细胞协同参与脂肪组织炎症发展，并通过自身攻击及表观遗传学机制导致肝损伤，促进NASH发病。由此得知CD8+T淋巴细胞可能成为NASH新的治疗靶点，未来继续深入研究CD8+T淋巴细胞在NASH中影响发病进程的具体机制有利于进一步指导临床治疗。
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关键词:
- 非酒精性脂肪性肝病 /
- CD8阳性T淋巴细胞 /
- 脂肪组织 /
- 炎症 /
- 表观基因组学
Abstract: Nonalcoholic steatohepatitis （NASH） is a liver disease closely associated with metabolic syndrome， and its pathogenesis includes insulin resistance， lipid metabolism disorders， and inflammatory response. This article briefly describes how CD8+ T cells exert a cytotoxic effect through the three pathways of the Fas-Fas ligand signaling pathway， the release of perforin and granzymes， and the secretion of tumor necrosis factor-α and other cytokines， and these mechanisms allow CD8+ T cells to specifically kill virus-infected cells and tumor target cells， thereby participating in immune regulation. At the same time， this article summarizes that CD8+ T cells promote the recruitment of macrophages cooperate with natural killer T cells to participate in the development of adipose tissue inflammation， and lead to liver injury through automatic attack and epigenetic mechanisms， finally promoting the pathogenesis of NASH. It is concluded that CD8+ T cells may become a new therapeutic target for NASH， and in-depth research on the specific mechanism of CD8+ T cells affecting the pathogenesis in NASH in the future may help to further guide clinical treatment. -
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