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作 者:尤丽芬[1,2] 俞富荣[1,2] 张文华[1,2] 冯东举 徐贤秀[1,2]
机构地区:[1]南京医科大学微生物学教研室 [2]南京大学医药生物技术国家重点实验室
出 处:《上海免疫学杂志》1999年第3期147-150,共4页Shanghai Journal of Immunology
摘 要:应用改良型TNFα(ITNFα)和IFNγ刺激小鼠腹腔巨噬细胞(MΦ)诱生一氧化氮(NO),并观察对细胞毒作用的影响。结果:IFNγ可激活小鼠腹腔MΦ产生小量NO,并伴随产生低度细胞毒活性,尤其是对经IFNγ处理的靶细胞(γL1210细胞)为显著。单用ITNFα刺激的MΦ,诱生NO不显著或微量,对靶细胞也无明显细胞毒作用。但ITNFα(100ng/ml)和IFNγ(50U/ml)共同刺激MΦ,可产生有意义量的NO(P<005),对γL1210细胞有显著细胞作用(P<001),而对未经IFNγ处理的靶细胞(L1210cels)无明显细胞毒作用。这可能是IFNγ促进MΦ诱生NO和靶细胞表面粘附分子的表达,加强效靶识别和结合,提高了对靶细胞的杀伤力。Effects of improved type of TNF(ITNF) and IFN on the induction of nitric oxide in murine macrophages and macrophagemediated cytotoxicity were investigatedThe ITNF was constructed by gene engineering techniques with deleting 38 Nterminal amino acid residues(SerSerSerArgThrPro) and replacing with 2 residues(LysArg)The results showed that murine macrophages incubated with IFN alone or with ITNF produced little of detectable NO,but they produced significant amounts of NO when cultured with a combination of IFN and ITNF(P<005)As to the macrophage mediated cytotoxicity,if macrophages were cultured with ITNF in combination with IFN,it was significantlyaurgmented in L1210 cells pretreated with IFN(P<001)Pretreatment of L1210 cells with IFN significantly increased their susceptibility to macrophage mediatedcytotoxicity owing to the increased NO production and the expression of cell adhesion molecules
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