Toll样受体4介导的Th2免疫在支气管哮喘中的作用  

Role of toll-like receptor 4-mediated Th2-immunity in bronchial asthma

作　　者：汪凤凤[1] 苗伟伟[1] 李红岩[1] 王文璐[1] 黄茂[1] 殷凯生[1] 周林福[1] 

机构地区：[1]南京医科大学第一附属医院呼吸内科,210029

出　　处：《中华哮喘杂志（电子版）》2011年第5期353-357,共5页Chinese Journal of Asthma(Electronic Version)

基　　金：国家自然科学基金(81170018;30570797;30400191);江苏省医学重点人才项目(RC2007043);江苏省六大人才高峰项目(06B035);人事部和教育部留学回国人员科技启动项目(200886;FD09);江苏省高校自然科学研究项目(11KJB320008);南京市科技计划项目(200901078)

摘　　要：支气管哮喘(简称哮喘)是一种以Th2优势免疫为特征的慢性气道炎症性疾病。Toll样受体4(TLR4)是表达在固有免疫细胞表面的模式识别受体,与病原体相关分子模式结合并启动细胞内信号转导。脂多糖介导的TLR4信号转导激活核转录因子NF-κB,引起固有免疫细胞活化。一方面,分泌多种促炎症细胞因子、参与炎症形成,并促进抗原递呈,引起初始型T细胞向Th1或Th2分化。另一方面,诱导协同刺激分子表达,启动特异性免疫应答。这两种效应在哮喘气道炎症、气道高反应性和气道重塑的发生与发展过程中起着重要作用。以TLR4信号通路作为靶点,有望为哮喘免疫治疗开辟新的途径。Bronchial asthma(asthma) is a T-helper type 2(Th2) immunity-biased chronic airway inflammatory disorder.Toll-like receptor 4(TLR4),a pattern recognition receptor expressed on the innate immune cells,combines with the pathogen-associated molecular pattern and initiates the signal transduction,leading to expression of the effector molecules.Lipopolysaccharide-mediated TLR4 signaling activates nuclear transcription factor NF-κB,resulting in activation of innate immune cells.On one hand,it secretes a series of inflammatory mediators,and promotes the antigen presentation,rendering the differentiation of naive T cells into either Th1 or Th2 phenotype.On the other hand,it induces the expression of costimulatory molecules,and triggers the specific immune response.Both effects play an important role in the pathogenesis of airway inflammation,hyperresponsiveness,and remodeling.It is promising for immunotherapy of asthma by targeting the TLR4 signaling pathway.

关 键 词：TOLL样受体4 核因子ΚB 信号转导 树突状细胞 免疫治疗 哮喘 

分 类 号：R56[医药卫生—呼吸系统]