实用肝脏病杂志 ›› 2012, Vol. 15 ›› Issue (5): 427-429.doi: 10.3969/j.issn.1672-5069.2012.05.0018

• 基础研究 • 上一篇    下一篇

MHV-3诱导的暴发性肝炎小鼠肝脏表达IL-9免疫细胞的变化*

朱琳, 陈韬, 宁琴   

  1. 430030 武汉市 华中科技大学附属同济医院感染性疾病研究所/感染病科
  • 收稿日期:2012-03-06 出版日期:2012-10-10 发布日期:2017-03-09
  • 通讯作者: 宁琴,E-mail:qning@tjh.tjmu.edu.cn
  • 作者简介:朱琳 女,28岁,博士研究生。主要从事病毒性肝炎免疫学机制研究。
  • 基金资助:
    国家自然科学基金重点项目(No.81030007); 国家自然科学基金(No.81100308)

Increased percentage of hepatic IL-9-secreting lymphocytes in MHV-3-induced fulminant hepatitis in mice

Zhu Lin, Chen Tao, Ning Qin.   

  1. Institute and Department of Infectious Diseases,Tongji Hospital,Tongji Medical College,Huazhong University of Science and Technology,Wuhan 430030,China
  • Received:2012-03-06 Online:2012-10-10 Published:2017-03-09

摘要: 目的 研究MHV-3病毒感染所致的暴发性肝炎小鼠肝脏T淋巴细胞亚群胞内细胞因子IL-9表达的变化,以探讨IL-9在该疾病模型中的作用。方法 利用MHV-3病毒诱导Balb/cJ小鼠暴发性肝炎模型,采用流式细胞术检测肝脏分泌IL-9的淋巴细胞亚群比例的变化。结果 随着MHV-3感染时间的延长,肝脏分泌IL-9的CD4+T细胞比例由感染前的1.87±1.36%于48小时升高到4.77±0.42%,差异显著(P<0.05);而分泌IL-9的CD4-CD8-(DN)T细胞比例则于感染后72小时达峰值7.83±3.30%,显著高于感染前(3.57±1.82,P<0.05)和24小时时(3.60±0.85,P<0.05)。结论 随着感染时间延长,肝脏分泌IL-9的CD4+T和CD4-CD8-(DN)T淋巴细胞显著升高,说明IL-9可能参与了MHV-3诱导的暴发性肝炎小鼠免疫诱导的肝脏损伤发病过程。

关键词: MHV-3, 暴发性肝炎, IL-9, DNT细胞

Abstract: Objective To investigate the changes of hepatic IL-9-secreting lymphocytes in MHV-3-induced fulminant hepatitis in mice for the analysis of involvement of IL-9 in the mechanisms of immune- mediated liver injury. Method MHV-3-induced fulminant hepatitis model was established in mice,and the percentage of hepatic IL-9-secreting T lymphocytes was determined by flow cytometry. Results The percentage of hepatic IL-9-producing CD4+T cells increased from 1.87±1.36% to 4.77±0.42% at 48h after viral inoculation(P<0.05),while the percentage of hepatic CD4-CD8-(DN) T cells who also expressed IL-9 at 72h after infection was 7.83±3.30%,which was significantly higher than that at 24h(P<0.05). Conclusion The increased expression of IL-9 from hepatic CD4+T and DNT lymphocytes may contribute to immune-mediated liver injury in MHV-3- induced fulminat hepatitis in mice.