Th17细胞与Treg细胞在支气管哮喘发病机制中的研究进展  

Thl7 cell and CD4^＋ CD25^＋ Treg in pathogenesis of asthma

作　　者：姚斌(综述)[1] 李敏(审校)[2] 

机构地区：[1]泸州医学院,泸州646000 [2]四川省人民医院儿科,成都610072

出　　处：《国际儿科学杂志》2012年第2期196-198,202,共4页International Journal of Pediatrics

摘　　要：近年来，众多研究发现支气管哮喘的发病机制已不能单纯用Th1／Th2平衡理论来解释，CD4^＋CD25^＋调节性T细胞和Thl7细胞及其细胞因子IL-10、IL-17、转化生长因子-β等与支气管哮喘发病明显相关。由于TH17细胞与CD4^＋CD25^＋调节性T细胞在功能上相互拮抗，而在分化上密切相关，因此这两种细胞的免疫失衡也是支气管哮喘发病的重要原因。糖皮质激素可通过维甲酸相关孤核受体γt信号途径降低IL-17的表达，还可以通过诱导转录因子Foxp3的表达调控CD4^＋CD25^＋调节性T细胞的分化和功能。Many studies have suggested that pathogenesis of asthma could no longer be interpreted merely by ＂Thl/Th2 balance＂ theory. CD4 ^＋ CD25^＋ Treg and Th17 cells, as well as their cytokines such as IL- l0, transforming growth factor-β, and IL-17, account for asthma. CD4^＋ CD25^＋ Treg and Th17 are functionally antagonistic to each other, and also go with each other during their differentiation. Therefore, immunity-unbalance of CD4^＋ CD25^＋ Treg and Thl7 is one of the most important factors that triggers asthma. Glucocorticoid has been shown to down regulate IL-17 expression by retinoic acid receptors γt signaling pathway, and regulate differentia- tion and function of CD4^＋ CD25^＋ Treg by inducing expression of transcription factor Foxp3, all of these are immuno-mechanisms of glucocorticoid in asthma treatment.

关 键 词：支气管哮喘 TREG细胞 发病机制 CD4^+CD25^+调节性T细胞 TH17细胞 转录因子FOXP3 转化生长因子-β Th1/Th2 

分 类 号：R562.25[医药卫生—呼吸系统]