首页> 中文期刊>中国免疫学杂志 >可诱导共刺激分子诱导骨髓来源不成熟树突状细胞特异性分泌IL-6

可诱导共刺激分子诱导骨髓来源不成熟树突状细胞特异性分泌IL-6

     

摘要

Objective :To determine whether ICOS could deliver any reverse signals through ICOSL expressed on mouse-derived immature dendritic cells (DCs ) and to detail their possible characteristics .Methods :The Surface phenotype molecules of DCs were determined by flow cytometry and the variation of cytokines was detected by ELISA .Real-time PCR was used for the evaluation of mRNA levels of cytokines , chemokines and their receptors .Results :High expression of MHC-Ⅱ ,CD80 ,CD86 and CD83 was induced on the surface of DCs when they were coincubated with ICOSIg or CHO cells expressing membrane-anchored ICOS .More intriguingly ,IL-6 was significantly and specifically elevated in these conditions .Conclusion :Our data ,for the first time ,provide some biological proofs showing that ICOS ,through binding ICOSL on the cell surface ,can deliver some reverse signals to immature DCs ,inducing a specific secretion of IL-6 by activating p38-MAPK signal pathway .%目的:分析可诱导共刺激分子(ICOS)可溶性融合蛋白(ICOSIg)能否向不成熟DCs传递逆向信号及其性质.方法:以流式细胞仪结合特异性抗体检测DCs表型分子改变;以ELISA检测培养上清细胞因子变化;以RT-PCR检测各组DCs细胞内细胞因子及受体、趋化因子等mRNA表达水平.结果:ICOSIg或膜锚定ICOS作用于不成熟DCs,均可诱导其高表达MHC-Ⅱ、CD80、CD86和CD83等表型分子;促进DCs特异性分泌IL-6.结论:ICOS作用于不成熟DCs表面的ICOSL可以向DCs细胞传递逆向信号,诱导DCs细胞高分泌IL-6,同时其表面重要的表型分子也上调,可能参与了DCs细胞免疫功能的调节,其信号转导机制可能涉及p38-MAPK通路.

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