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很久以来,人们已认识到特异性T细胞介导的免疫反应激活巨噬细胞(Mφ),可获得强有力的杀伤多种感染性病原微生物的功能。Mφ激活后产生大量的分泌产物与杀伤微生物的活性有关。多年来,研究人员一直无法鉴定在介导淋巴细胞激活的Mφ的细胞毒中直接的和非特异性效应分子。最近在以肿瘤作靶细胞的研究中揭示,激活的Mφ通过精氨酸依赖途径产生氮氧化合物具有细胞毒作用:一是抑制DNA复制;二是抑制细胞呼吸,都与影响细胞内Fe含量有关。肿瘤细胞线粒体电子传递系统相邻的两个氧化还原酶[NADH-辅酶Q氧化还原酶(复合物I)
It has long been recognized that the specific T cell-mediated immune response activates macrophages (Mφ), which can potently kill many infectious pathogenic microorganisms. Mφ activation produces a large number of secreted products and antimicrobial activity. For years, researchers have been unable to identify direct and non-specific effector molecules in cytotoxic Mφ that mediate lymphocyte activation. Recent studies using tumors as target cells revealed that activated Mφ has the cytotoxic effect of producing oxynitrides via an arginine-dependent pathway: one is inhibition of DNA replication; the other is inhibition of cellular respiration, both of which are associated with effects on intracellular Fe content . Two oxidoreductases [NADH-coenzyme Q oxidoreductase (Complex I)) adjacent to the tumor cell mitochondrial electron transport system