期刊文献+

HBeAg诱导的免疫激活和免疫抑制在慢性乙型肝炎中的作用 被引量:1

Role of HBeAg-induced immune activition and immunosuppression in chronic hepatitis B
下载PDF
导出
摘要 HBV感染诱导的慢性乙型肝炎是导致肝硬化和肝癌的重要危险因素。半个世纪前,HBeAg在HBV感染者血清中首次被发现,尽管HBeAg并不参与HBV在肝细胞中的感染或复制,但其已被证实可干扰宿主先天性和适应性免疫反应,在慢性HBV感染的过程中发挥着重要的免疫激活和免疫抑制作用。HBV对于感染的肝细胞并没有细胞毒性,免疫应答介导的抗病毒作用和炎症反应决定HBV是否被清除或者诱导肝脏炎症相关疾病。因此,本文对HBeAg的形成及其在慢性HBV感染中引起的免疫激活和免疫抑制机制进行综述,重点论述HBeAg对先天免疫和适应性免疫细胞所引起的不同免疫效应,阐述了其诱导免疫反应的两面性,并探讨HBeAg在慢性HBV感染不同阶段间的转换作用。 Chronic hepatitis B induced by HBV infection is a significant risk factor leading to liver cirrhosis and liver cancer.Half a century ago,HBeAg was first discovered in the serum of HBV infected individuals,and although HBeAg does not participate in HBV infection or replication in hepatocytes,studies have shown that it can interfere with the innate and adaptive immune responses of the host and play an important role in immune activation and immunosuppression during chronic HBV infection.HBV has no cytotoxicity to the infected hepatocytes,and the antiviral action and inflammatory response mediated by immune response determine whether HBV is cleared or induces liver inflammation-related diseases.Therefore,this article reviews the formation of HBeAg and its immune activation and immunosuppression mechanisms in chronic HBV infection,with a focus on the different immune effects caused by HBeAg on innate immune and adaptive immune cells,and this article also elaborates on the dual role of HBeAg in inducing immune responses and explores the conversion role of HBeAg in different stages of chronic HBV infection.
作者 李欣阳 涂正坤 LI Xinyang;TU Zhengkun(Laboratory of Tumor Immunology,The First Hospital of Jilin University,Changchun 130021,China)
出处 《临床肝胆病杂志》 CAS 北大核心 2024年第5期1026-1031,共6页 Journal of Clinical Hepatology
基金 吉林省科技发展计划项目自然科学基金(20190201245JC)。
关键词 乙型肝炎 慢性 乙型肝炎E抗原 免疫激活 免疫抑制 Hepatitis B,Chronic Hepatitis B e Antigens Immune Activation Immune Suppressive
  • 相关文献

参考文献3

二级参考文献4

共引文献18

同被引文献15

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部