摘要
目的：观察PAF对T细胞 PKC激活的调节作用。方法：以 CD3mAb（30 ng/ml）或PMA（50 ng/ml）/ionomycin（500 ng/ml）活化 T细胞。T细胞增生以3H胸腺嘧啶掺入法测定，IL-2生成用 MTT法测定，11-2R（CD25）表达以流式细胞仪测定，PKC活性用 Hauschildt所述方法测定。结果：PAF抑制由 CD3mAb诱导的 T-细胞增生、IL-2生成、CD25的表达和PKC的激活。虽然PAF对 PMA/ionomycin诱导的 T-细胞增生和 CD25的表达也具有抑制作用，但是，对 IL-2生成的抑制作用并不显著。结论：PAF除抑制PKC激活外，对PKC激活之前的信号传导过程亦有调节作用。
Abstract Objective: To investigate the regulatory effect of PAF on early events in signal transduction during T-cell activation. Methods:T-cell activation was achieved by stimulation of human T cells with CD3 mAb or PMA/ionomycin in the presence or absence of PAF. T cell Pro-liferatilon was determined by 3 H-thymidine incorporation, IL-2 production was measured by MTT method, IL-2R(CD25)expression was evaluatedby flow cytometry and,PKC activity was assayed by the method described by Hauschildt. Results:PAF inhibited CD3 mAb-induced T-cell pro-liferation, IL-2 production and CD25 expression. AIthough it inhibited T-cell proliferation and IL-2 production induced by PMA/ionomycin, PAFfailed to inhibit IL-2 production induced by PMA/ionomycin.The translocation of PKC was also inhibited by PAF if T cells were activated byCD3mAb. Conclusion: PAF inhibits T-cell activation via its inhibitory effect on PKC activation. Its differential effect on IL-2 production suggeststhat PAF regulatory more early events in signal transduction such as the activation of phospholipase C γ-1.
出处
《中国免疫学杂志》
CAS
CSCD
北大核心
2002年第5期322-324,共3页
Chinese Journal of Immunology
关键词
血小板活化因子
PAF
蛋白激酶
PKC
T细胞活化
淋巴细胞
Keywords:Platelet-activating factor (PAF) Signal transduction Protein kinase C(PKC) T-cell activation
