乙型肝炎eAg原通过将CD4 + CD25-T细胞转化为CD4 + CD25 + Foxp3 +

StephenW

Hepatitis B envelope antigen increases Tregs by converting CD4+CD25 - T cells into CD4 + CD25 + Foxp3 + Tregs
Rui Tang  1 , Zhigang Lei  1 , Xinpeng Wang  1 , Qianqian Qi  1 , Jingjing He  1 , Dan Liu  1 , Xiaoxian Wang  1 , Xiaojun Chen  1 , Jifeng Zhu  1 , Yalin Li  1 , Sha Zhou  1 , Chuan Su  1
Affiliations
Affiliation

    1
    State Key Laboratory of Reproductive Medicine, Department of Pathogen Biology and Immunology, Jiangsu Key Laboratory of Pathogen Biology, Center for Global Health, Nanjing Medical University, Nanjing, Jiangsu 211166, P.R. China.

    PMID: 32855720 PMCID: PMC7444405 DOI: 10.3892/etm.2020.9107

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Abstract

Hepatitis B virus (HBV) can establish a lifelong chronic infection in humans, leading to liver cirrhosis, liver failure and hepatocellular carcinoma. Patients with chronic hepatitis B (CHB) exhibit a weak virus-specific immune response. Regulatory T cells (Tregs) play a key role in regulating the immune response in patients with CHB. Patients with hepatitis B envelope antigen (HBeAg)-positive CHB harbored a higher percentage of Tregs in their peripheral blood than those with HBeAg-negative CHB. However, whether and how HBeAg manipulates the host immune system to increase the population of Tregs remains to be elucidated. The present manuscript describes a preliminary immunological study of HBeAg in a mouse model. Multiple potential CD4+ T cell epitopes in HBeAg were identified using Immune Epitope Database consensus binding prediction. It was demonstrated that HBeAg treatment increased the numbers of Tregs in mouse spleens in vitro and in vivo. Furthermore, it was indicated that the HBeAg-mediated increase in Tregs occurred through the conversion of CD4+CD25- T cells into CD4+CD25+Foxp3+ Tregs. Additionally, in vitro study illustrated that HBeAg stimulated murine spleen cells to produce increased transforming growth factor-β, which is required to enable HBeAg to convert T cells into Tregs. The results of the present study may provide further evidence of the effect of HBeAg on Tregs and aid in the development of novel HBeAg-based immunotherapy for CHB.

Keywords: HBV; HBeAg; chronic infection; immune regulation; regulatory T cell.

StephenW

乙型肝炎包膜抗原通过将CD4 + CD25-T细胞转化为CD4 + CD25 + Foxp3 + Tregs来提高Tregs
汤锐1，雷志刚1，王新鹏1，钱谦1，何晶晶1，刘丹1，王小贤1，陈晓军1，朱继峰1，李亚琳1，沙洲1，川苏1
隶属关系
联系

    1个
    南京医科大学全球卫生研究中心，病原生物学与免疫学系，生殖生物学国家重点实验室，江苏省病原生物学重点实验室，江苏南京211166。

    PMID：32855720 PMCID：PMC7444405 DOI：10.3892 / etm.2020.9107

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抽象

乙型肝炎病毒（HBV）可以在人类中建立终生的慢性感染，导致肝硬化，肝衰竭和肝细胞癌。慢性乙型肝炎（CHB）患者表现出弱的病毒特异性免疫反应。调节性T细胞（Tregs）在调节CHB患者的免疫应答中起关键作用。乙型肝炎包膜抗原（HBeAg）阳性的CHB患者外周血中Treg的百分比高于HBeAg阴性的CHB。但是，HBeAg是否以及如何操纵宿主免疫系统以增加Tregs的数量仍有待阐明。本手稿描述了HBeAg在小鼠模型中的初步免疫学研究。使用免疫表位数据库共有结合预测，鉴定了HBeAg中多个潜在的CD4 + T细胞表位。证实了HBeAg治疗在体外和体内增加了小鼠脾脏中Treg的数量。此外，表明HBeAg介导的Treg的增加通过CD4 + CD25-T细胞转化为CD4 + CD25 + Foxp3 + Treg而发生。此外，体外研究表明，HBeAg刺激鼠脾细胞产生增加的转化生长因子-β，这是使HBeAg将T细胞转化为Treg所必需的。本研究的结果可能为HBeAg对Treg的作用提供进一步的证据，并有助于开发基于HBeAg的新型CHB免疫疗法。

关键字：HBV；乙肝抗原慢性感染；免疫调节调节性T细胞。

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