氢化可的松对人外周血来源树突状细胞的诱导凋亡作用研究  

The Study on Apoptosis of Dendritic Cell from Peripheral Blood Induced by Hydrocortisone

作　　者：谢炜[1] 王月丹[1] 邱玉华[1] 徐颖 张学光[1] 

机构地区：[1]苏州医学院生物技术研究所,苏州215007

出　　处：《上海免疫学杂志》2000年第6期337-340,共4页Shanghai Journal of Immunology

基　　金：国家自然科学基金!资助项目 (39870 82 5 );江苏省科委重点资助!项目 (BJ9810 0 )

摘　　要：旨在探讨氢化可的松对人外周血单核细胞来源树突状细胞 (DC )的凋亡诱导作用及其表型、功能的变化 ;采用细胞因子体外诱导人外周血来源DC ,加入不同浓度的氢化可的松进行培养 ;以细胞计数、PI染色测定细胞周期、间接荧光表型分析、ELISA法测定DC分泌的IL 12和3H TdR掺入测定DC对T细胞的激发作用 ;实验结果表明 ,外周血贴壁的单核细胞在细胞因子的诱导下可以分化为成熟的DC ,不同浓度 (2 μg/ml～ 5 0 μg/ml)的氢化可的松可下调DC表达的CD80和HLA DR分子 (分别下降 41 1%和 10 9% ) ,并使其分泌IL 12的能力明显下降 (由 38 1pg下降为 0 ) ,DC对自体T细胞的激发功能明显降低 ,而且一定浓度的氢化可的松还可以使DC发生凋亡 (凋亡率可达 5 6 6 % )。糖皮质激素不仅通过下调DC表达的协同刺激分子及其分泌的IL 12从而影响DC对T细胞的激发作用 ,而且可以直接诱导DC发生凋亡 ,从而下调免疫应答的发生。To study the effect of hydrocortisone on phenotype,function and apoptosis of dendritic cell (DC) from peripheral blood monocyte (PBMC),DC induced from PBMC by cytokines were co cultured with different concentration of hydrocortisone,and the treated DC were counted and phenotyped by cytometry analysis Cell cycle of DC was analyzed by PI dye;and IL 12 concentration of the DC supernatant was determined by ELISA The effect of DC to stimulate T cells was processed by MLR and 3H TdR Results showed that hydrocortisone (2μg/ml to 50μg/ml) can down regulate the expression of CD80 and HLA DR of monocyte derived DC,declined 41 1% and 10 9% respectively The capability of DC to secrete IL 12 deduced obviously (from 38 1pg/ml to 0);and the function of DC to stimulate autologous T cells was declined after treatment with hydrocortisone as well Furthermore,hydrocortisone of certain concentration can induced DC to apoptosis (the rate of apoptosis was 56 6% after co cultivation with 50μg/ml of hydrocortisone) It concludes that hydrocortisone can not only effect the function of DC to stimulate T cell by down regulating the expression of costimulatory of DC and the secretion of IL 12 of DC,but also can induce the apoptosis of DC as well

关 键 词：糖皮质激素 树突状细胞 凋亡 氢化可的松 

分 类 号：R977.1[医药卫生—药品] R329.28[医药卫生—药学]