创伤后巨噬细胞对T细胞白介素2及白介素2受体α基因表达的直接接触抑制作用

INHIBITION OF T CELLS INTERLEUKIN 2 AND INTER- LEUKIN 2 RECEPTOR a GENE EXPRESSION BY DIRECT CONTACT WITH MACROPHAGES AFTER TRAUMA

以25μg/ml的丝裂霉素C处理巨噬细胞30min,可阻断巨噬细胞白介素1(IL-1)、白介素6(IL-6)、肿瘤坏死因子(TNF)及前列腺素E_2(PGE_2)的合成与分泌。创伤小鼠巨噬细胞经丝裂霉素C处理后,可明显抑制正常T细胞白介素2(IL-2)mRNA及IL-2受体(IL-2R)αmRNA水平,并增强Ts细胞的抑制活性。去除T细胞中Ts细胞可使巨噬细胞的抑制作用消失。表明创伤后巨噬细胞可通过直接的细胞接触方式抑制T细胞IL-2及IL-2 Rα的基因表达,且这一作用是通过增加Ts细胞活性而实现的。

Treating macrophages with 25 Jig/ml mitomycin-C for 30 min could abrogate the production and secretion of interleukin l(IL-l), interleukin 6(IL-6), tumour necrosis factor (TNF) and prostaglandift E2(PGE2). Macrophages frbm traumatized mice toeaiea wtth mitomycin-C could suppress obviously IL-2 mRNA and IL-2Ra mRNA levels of normal T cells, while elevate su-ppressive action of Ts cells. Removal of Ts cells from T cells could abolish the inhibition of macrophages. It is suggested that macrophages post trauma can depress IL-2 and JL-2Rα gene expression in T cells by direct cell to cell contact, and this effect is mediated by increasing the action of Ts cells.