Th1/Th2细胞因子处理的树突状细胞在过敏性气道炎症中作用  

Roles of Th1/Th2 cytokine-treated dendritic cells in allergic airway inflammation

作　　者：夏俊波[1] 宋云熙[1] 曾雪峰[1] 王彦[1] 王长征[1] 

机构地区：[1]第三军医大学新桥医院全军呼吸内科研究所,重庆400037

出　　处：《免疫学杂志》2008年第2期195-197,201,共4页Immunological Journal

基　　金：国家自然科学基金资助项目(30640094)

摘　　要：目的探讨Th1/Th2细胞因子IL-4或IFNγ对树突状细胞生物学性状的影响以及经IL-4或IFNγ处理后的树突状细胞在过敏性气道炎症中的作用。方法体外扩增小鼠骨髓来源的树突状细胞,采用流式细胞术检测IL-4或IFNγ对树突状细胞表型的影响以及观察IL-4或IFNγ处理的树突状细胞对T细胞的作用;观察IL-4或IFNγ处理的树突状细胞过继卵蛋白致敏小鼠肺组织病理特点和支气管肺泡灌洗液细胞类型。结果IL-4或IFNγ处理的树突状细胞表达CD80和MHCⅡ均明显增加并呈剂量依赖性;IL-4处理的树突状细胞显著增加T细胞分泌IL-4,而IFNγ处理的树突状细胞显著增加T细胞分泌IL-4和IFNγ;IL-4或IFNγ处理的树突状细胞过继小鼠肺组织可见典型的过敏性气道炎症改变,支气管肺泡灌洗液细胞类型与哮喘组无显著差异。结论IL-4活化的树突状细胞诱导Th2免疫反应,IFNγ活化的树突状细胞诱导Th1和Th2免疫反应,而且IFNγ并未改善过敏性气道炎症。Objective To explore the effects of IL-4/IFNγ on dendritic cell and the role of IL-4/IFNγ-treated dendritic cell in asthmatic airway inflammation. Methods Dendritic cells were generated from mouse bone barrow in vitro at the present of GM-CSF. Flow cytometry was used to detect the expressions of CD80 and MHC Ⅱ on dendritic cells treated by different dose of IL-4/IFNγ. ELISA was used to detect the Th1/Th2 cytokines secreted by these dendritic cells-activated T cells. Pathological changes and BALF cell types of OVA-sensitized mouse transferred by IL-4/IFNγ-treated dendritic cell were observed. Results The expressions of CD80 and MHC Ⅱ on IL-4/IFNγ-treated dendritic cells were increased in a dose-depend manner. IL-4 secreted by T cells activated by IL-4-treated dendritic cells was significantly increased, meanwhile IL-4 and IFNγ secreted by T cells activated by IENγ-treated dendritic cells were significantly increased. Typical asthmatic pathological changes were found in lung tissues of adoptive transferred mouse. The BALF cell types were not significantly changed compared with asthma group. Conlusion IL-4-treated dendritic cells induce Th2-like response and IFN-γ-treated dendritic cells induce both Thl and Th2-like response and never alter the existed allergic airway inflammation.

关 键 词：树突状细胞 IL-4 IFNΓ 

分 类 号：R392[医药卫生—免疫学]