在乙型肝炎病毒相关的终末期肝病中，新型 T 淋巴细胞亚群 C

StephenW

在乙型肝炎病毒相关的终末期肝病中，新型 T 淋巴细胞亚群 CD3 + CD4 - CD7 + CD57 - T 细胞的频率降低可能导致疾病进展
于雪平 1 2 , 郑宜娟 1 , 曾大武 2 3 , 周永军 4 , 孙建 2 5 , 米龙 1 , 张华堂 1 , 郑敏辉 1 , 黄志鹏 1 , 林文武 1 , 毛日成 2 , 张继明 2 , 郑春福 6 7 , 苏志军 1
隶属关系
隶属关系

    1
    福建医科大学附属泉州第一医院感染科，泉州 362000
    2
    复旦大学华山医院国家传染病医学中心传染病与生物安全应急研究所上海市传染病与生物安全应急响应重点实验室传染病科, 上海, 200040
    3
    福建医科大学附属第一医院肝病中心，福州 350005
    4
    闽南科技大学生命科学与化学学院生物工程与生物技术研究所, 泉州, 362000
    5
    皖南医学院第一附属医院感染科,芜湖,241000
    6
    福建医科大学基础医学院免疫学系，福州
    7
    加拿大阿尔伯塔省卡尔加里市卡尔加里大学微生物学、免疫学和传染病学系。

    PMID：36068190 DOI：10.1002/jmv.28129

抽象的

CD7 和 CD57 与 CD8+ T 细胞的分化和功能阶段有关。然而，在慢性乙型肝炎病毒 (HBV) 感染患者，尤其是终末期肝病患者中，它们在 CD8+ T 细胞中的联合作用仍不清楚。通过 Luminex 测定和 ELISA 分析来自健康志愿者和慢性乙型肝炎患者的血液样本，以测量血浆细胞因子水平。此外，重组 IL-22 用于刺激健康志愿者的外周血单个核细胞，并通过流式细胞术研究 CD3+ CD4- CD7+ CD57- T 细胞的频率和细胞凋亡率。终末期肝病患者，尤其是急性至慢性肝功能衰竭患者，CD3+ CD4- CD7+ CD57- T 细胞频率降低。此外，CD3+ CD4- CD7+ CD57- T 细胞的患病率与疾病严重程度、预后和并发症（腹水）呈负相关。我们还观察到 IL-22 以剂量依赖性方式促进细胞凋亡并导致 CD3+ CD4- CD7+ CD57- T 细胞数量减少。 CD3+ CD4- CD7+ CD57- T 细胞表现出 BTLAhigh CD25high CD127high 免疫抑制表型，并表现出低 IFN-γ、TNF-α、颗粒酶 A 和穿孔素表达水平。本研究结果将阐明 HBV 相关终末期肝病的发病机制，并有助于确定新的药物靶点。本文受版权保护。版权所有。

关键词：慢加急性肝衰竭 CD57； CD7; CD8+T 细胞；乙型肝炎病毒。

本文受版权保护。版权所有。

StephenW

Decreased frequency of a novel T-lymphocyte subset, CD3 + CD4 - CD7 + CD57 - T cells, in hepatitis B virus-related end-stage liver disease might contribute to disease progression
Xueping Yu  1   2 , Yijuan Zheng  1 , Dawu Zeng  2   3 , Yongjun Zhou  4 , Jian Sun  2   5 , Milong Su  1 , Huatang Zhang  1 , Minhui Zheng  1 , Zhipeng Huang  1 , Wenwu Lin  1 , Richeng Mao  2 , Jiming Zhang  2 , Chunfu Zheng  6   7 , Zhijun Su  1
Affiliations
Affiliations

    1
    Department of Infectious Diseases, Fujian Medical University Affiliated First Quanzhou Hospital, Quanzhou, 362000, China.
    2
    Department of Infectious Diseases, Shanghai Key Laboratory of Infectious Diseases and Biosafety Emergency Response, Shanghai Institute of Infectious Diseases and Biosecurity, National Medical Center for Infectious Diseases, Huashan Hospital, Fudan University, Shanghai, 200040, China.
    3
    Department of Liver Center, the First Hospital Affiliated to Fujian Medical University, Fuzhou, 350005, China.
    4
    Institute of Bioengineering and Biotechnology, College of Life Sciences and Chemistry, Minnan Science and Technology University, Quanzhou, 362000, China.
    5
    Department of Infectious Diseases, the First Hospital Affiliated to Wannan Medical College, Wuhu, 241000, China.
    6
    Department of Immunology, School of Basic Medical Sciences, Fujian Medical University, Fuzhou, China.
    7
    Department of Microbiology, Immunology and Infectious Diseases, University of Calgary, Calgary, Alberta, Canada.

    PMID: 36068190 DOI: 10.1002/jmv.28129

Abstract

CD7 and CD57 are related to the differentiation and functional stages of CD8+ T cells. However, the role of their combined presence in CD8+ T cells in patients with chronic hepatitis B virus (HBV) infection, especially those with end-stage liver disease, remains unclear. Blood samples from healthy volunteers and patients with chronic hepatitis B were analyzed via Luminex assay and ELISA to measure plasma cytokine levels. Further, recombinant IL-22 was used to stimulate peripheral blood mononuclear cells from healthy volunteers, and the frequency of CD3+ CD4- CD7+ CD57- T cells and apoptosis rates were investigated via flow cytometry. Patients with end-stage liver disease, particularly those with acute to chronic liver failure, showed decreased CD3+ CD4- CD7+ CD57- T cell frequency. Furthermore, the prevalence of CD3+ CD4- CD7+ CD57- T cells was negatively correlated with disease severity, prognosis, and complications (ascites). We also observed that IL-22 promoted apoptosis and brought about a decrease in the number of CD3+ CD4- CD7+ CD57- T cells in a dose-dependent manner. CD3+ CD4- CD7+ CD57- T cells displayed a BTLAhigh CD25high CD127high immunosuppressive phenotype and showed low IFN-γ, TNF-α, granzyme A, and perforin expression levels. The present findings will elucidate the pathogenesis of HBV-related end-stage liver disease and aid the identification of novel drug targets. This article is protected by copyright. All rights reserved.

Keywords: Acute-on-chronic liver failure CD57; CD7; CD8+T cells; Hepatitis B virus.

This article is protected by copyright. All rights reserved.