微生物与感染
2024年11月28日 星期四   首页 |  主编心语 |  期刊介绍 |  编委阵容 |  投稿指南 |  出版道德 |  期刊订阅 |  联系我们 | English
微生物与感染  2017, Vol. 12 Issue (5): 279-286    
  论著 本期目录 | 过刊浏览 | 高级检索 |
白细胞介素23在呼吸道合胞病毒感染致Th1、Th2及Th17细胞分化中的作用及机制
冯净净,陈家君,王盛美,揭志军
复旦大学附属上海市第五人民医院呼吸科,上海 200240
Role of interleukin 23 in facilitating Th1, Th2 and Th17 differentiation after respiratory syncytial virus infection
FENG Jingjing, CHEN Jiajun, WANG Shengmei, JIE Zhijun
Department of Respiratory Medicine, Shanghai Fifth People’s Hospital, Fudan University, Shanghai 200240, China
全文: PDF (982 KB)   HTML (0)
输出: BibTeX | EndNote (RIS)      
摘要: 本研究旨在探讨白细胞介素23(interleukin 23,IL-23)在呼吸道合胞病毒(respiratory syncytial virus,RSV)感染支气管上皮细胞BEAS-2B后对Th1、Th2和Th17细胞分化的影响及作用机制。将RSV感染BEAS-2B后的上清液与淋巴细胞共孵育,并分别阻断IL-23受体(IL-23 receptor,IL-23R)、IL-23p19亚基及p38丝裂原活化蛋白激酶(p38 mitogen-activated protein kinase,p38 MAPK)信号通路。应用酶联免疫吸附试验(enzyme-linked immunosorbent assay,ELISA)检测上清液中细胞因子γ干扰素(interferon γ,IFN-γ)、IL-4、IL-17的浓度。同时,应用实时聚合酶链反应(polymerase chain reaction,PCR)检测相关转录因子(t-bet、gata3、rorγt)和信号转导子(stat4、stat6、stat3)的表达。结果显示,RSV感染后IFN-γ、IL-4和IL-17蛋白表达上调,转录因子及信号转导子的表达也有所增加。阻断IL-23和p38 MAPK信号通路后,Th1、Th2和Th7细胞分泌的细胞因子及转录因子表达均明显下降。结果提示,阻断IL-23后可在基因转导层面抑制RSV感染上皮细胞后诱导的Th1、Th2和Th17细胞分化,此过程可能与p38 MAPK信号通路有关。

服务
把本文推荐给朋友
加入我的书架
加入引用管理器
E-mail Alert
RSS
作者相关文章
冯净净
陈家君
王盛美
揭志军
关键词 呼吸道合胞病毒白细胞介素23受体白细胞介素23 p19亚基p38丝裂原活化蛋白激酶信号通路T辅助细胞转录因子    
Abstract:The present paper aims to investigate the role of interleukin 23 (IL-23) in facilitating Th1, Th2 and Th17 differentiation during respiratory syncytial virus (RSV) infection of epithelial cells (BEAS-2B). Lymphocytes were treated by supernatants from BEAS-2B cells with RSV or mock infection. Then they were blocked by specific anti-IL-23R antibody, anti-IL-23p19 antibody and p38 mitogen-activated protein kinase (MAPK) inhibitor (SB203580). The concentrations of cytokines such as interferon γ (IFN-γ), IL-4 and IL-17 were detected by enzyme-linked immunosorbent assay (ELISA). The mRNA expressions of transcription factors (t-bet, gata3, rorγt), signal transducers (stat4, stat6, stat3) were determined by real-time polymerase chain reaction (PCR). The results showed that the concentrations of cytokines (IFN-γ, IL-4 and IL-17) were significantly increased after RSV infection, accompanied with the enhanced expressions of transcription factors. However, these cytokines and transcription factors were significantly decreased when IL-23 pathway was blocked by antibodies. The blockage of p38 MAPK signal pathway showed the same results. The results suggest that IL-23 could facilitate Th1, Th2 and Th17 differentiation in RSV-infected BEAS-2B cells, which might be associated with p38 MAPK signal pathway.

Key wordsRespiratory syncytial virus    Interleukin 23 receptor;Interleukin 23 p19 subunit    p38 mitogen-activated protein kinase signal pathway    T helper cell    Transcription factor
基金资助:上海市闵行区自然科学基金(2014MHZ056),上海市卫生和计划生育委员会科研课题(20164Y0264)

通讯作者: 揭志军   
引用本文:   
冯净净,陈家君,王盛美,揭志军. 白细胞介素23在呼吸道合胞病毒感染致Th1、Th2及Th17细胞分化中的作用及机制[J]. 微生物与感染, 2017, 12(5): 279-286.
FENG Jingjing, CHEN Jiajun, WANG Shengmei, JIE Zhijun. Role of interleukin 23 in facilitating Th1, Th2 and Th17 differentiation after respiratory syncytial virus infection. JOURNAL OF MICROBES AND INFECTIONS, 2017, 12(5): 279-286.
链接本文:  
http://jmi.fudan.edu.cn/CN/     或     http://jmi.fudan.edu.cn/CN/Y2017/V12/I5/279

版权所有 © 2008 《微生物与感染》编辑部
地址:上海市医学院路138号 邮编:200032
Tel:021-54237633 Fax:021-64434224    E-mail:jmi@fudan.edu.cn
本系统由北京玛格泰克科技发展有限公司设计开发  技术支持:support@magtech.com.cn