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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。
The purpose of this study was to investigate the effects of hydrocortisone on the apoptosis of human monocyte-derived dendritic cells (DCs) and their phenotypes and functions. Cytokines were used to induce DCs from human peripheral blood in vitro. Hydrocortisone were cultured in vitro. The cell cycle and indirect fluorescent phenotype were determined by cell counting and PI staining. IL 12 and 3H TdR secreted by DC were measured by ELISA. The results showed that DCs stimulated T cells by DCs. Peripheral blood adherent mononuclear cells can differentiate into mature DCs induced by cytokines. Hydrocortisone at different concentrations (2 μg / ml ~ 50 μg / ml) can down-regulate DCs expressing CD80 and HLA DR molecules (Decreased by 41 1% and 109% respectively), and significantly decreased its ability to secrete IL-12 (from 381 pg to 0). DC had a markedly decreased ability to stimulate autologous T cells, and a certain concentration of hydrocortisone DC can also make the apoptosis (up to 566% apoptosis rate). Glucocorticoid not only affects the DC stimulating effect on T cells but also directly induces the apoptosis of DCs by down-regulating costimulatory molecules expressed by DCs and their secretion of IL-12, thereby reducing the occurrence of immune responses.