CTLA4Ig融合蛋白体外免疫抑制作用机制探讨  

Investigation on the in vitro Mechanism of Immunosuppression by Fusion Protein CTLA4Ig

作　　者：周璟[1] 马宝骊[1] 张家胜[2] 王利[1] 韩晓枫[1] 张继英[1] 柏峻[1] 

机构地区：[1]上海第二医科大学上海市免疫学研究所,上海200025 [2]复旦大学医学院手外科研究所,上海200040

出　　处：《上海免疫学杂志》2001年第4期207-209,213,共4页Shanghai Journal of Immunology

摘　　要：本文在建立EAEWistar大鼠模型的基础上 ,借助MBP特异反应的T细胞 ,体外探讨CTLA4Ig免疫抑制作用。实验结果发现 ,CTLA4Ig (10 μg/ml)可完全抑制MBP反应的大鼠T细胞增殖 ,而外源性IL 2的同时加入可恢复T细胞针对MBP的增殖反应。FACS检测经CTLA4Ig处理的T细胞表面仍有少量IL 2R的表达 ,且CTLA4Ig能诱导T细胞凋亡。RT PCR结果显示CTLA4Ig能明显抑制IL 2mRNA的表达 ,轻度抑制IFN γmRNA和TNF αmRNA的表达 ,而对IL 10mRNA的表达无明显影响。The aim of this study was to investigate the in vitro mechanism of immunosuppression by fusion protein CTLA4Ig by means of MBP reactive rat T cells Experimental results showed that CTLA4Ig (10 μg/ml) could totally suppress rat MBP reactive T cell proliferation,and the addition of exogenous IL 2 could reverse the inhibitory effect Treatment with CTLA4Ig reduced the expression of IL 2 receptor on T cells and decreased the synthesis IL 2,IFN γ,TNF α but had no effect on the synthesis of IL 10 Meanwhile CTLA4Ig could also induce the T cell apoptosis in vitro The results of this study provide evidence for potenial application

关 键 词：CTLA4IG 实验性自身免疫性脑脊髓炎 髓鞘碱性蛋白 免疫抑制 

分 类 号：R515.2[医药卫生—内科学] R392.11[医药卫生—临床医学]