糖皮质激素诱导的肿瘤坏死因子受体在调节性T细胞的表达及功能  

Expression of Glucocorticoid-induced Tumor Necrosis Factor Receptor and Their Function on Regulatory T Cells

作　　者：孙甲峰[1] 李向培[1] 

机构地区：[1]安徽医科大学附属省立医院风湿免疫科,合肥230001

出　　处：《中华临床免疫和变态反应杂志》2011年第3期238-242,共5页Chinese Journal of Allergy & Clinical Immunology

基　　金：安徽省自然科学基金(090413129)

摘　　要：糖皮质激素诱导的肿瘤坏死因子受体(GITR)是肿瘤坏死因子家族成员,在调节性T(Treg)细胞组成性高表达。自身免疫炎症过程中GITR的表达增加,参与调节Treg细胞活性并进一步诱导效应T细胞活化。GITR配体(GITRL)使GITR活化后导致Treg细胞的抑制功能下降。另外,GITR与多种细胞的凋亡相关,但GITR信号在机体免疫系统中的作用及GITR与T细胞之间的关系目前仍不清楚。The glucocorticoid-induced tumor necrosis factor receptor（GITR,also known as TNFRSF18） a member of the TNF-nerve growth factor receptor gene superfamily was found in dexamethasone（DEX） induced cells.The expression of GITR was increased in autoimmune and inflammatory diseases and involved in the regulation of regulatory T cells.GITR-GITRL interaction could inhibit the function of regulatory T cells.In addition,GITR was related with cell apoptosis,but the role of GITR signaling in immune system has been unclear.

关 键 词：糖皮质激素诱导肿瘤坏死因子受体 调节性T细胞 凋亡 

分 类 号：R965[医药卫生—药理学]