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
出处
《上海免疫学杂志》
CSCD
北大核心
1999年第3期147-150,共4页
Shanghai Journal of Immunology
