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  

Role of interleukin 23 in facilitating Th1,Th2 and Th17 differentiation after respiratory syncytial virus infection

作　　者：冯净净 陈家君 王盛美 揭志军 

机构地区：[1]复旦大学附属上海市第五人民医院呼吸科,上海200240

出　　处：《微生物与感染》2017年第5期279-286,共8页Journal of Microbes and Infections

基　　金：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)

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-23receptor,IL-23R)、IL-23p19亚基及p38丝裂原活化蛋白激酶(p38mitogen-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(interferonγ,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(tbet、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。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-2 B）.Lymphocytes were treated by supernatants from BEAS-2 Bcells with RSV or mock infection.Then they were blocked by specific anti-IL-23 Rantibody,anti-IL-23 p19 antibody and p38 mitogen-activated protein kinase（MAPK）inhibitor（SB203580）.The concentrations of cytokines such as interferonγ（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 significantlydecreased 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-2 Bcells,which might be associated with p38 MAPK signal pathway.

关 键 词：呼吸道合胞病毒 白细胞介素23受体 白细胞介素23p19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 

分 类 号：R373[医药卫生—病原生物学]