Boraschi D, Ghezzi P, Salmona M, Tagliabue A
Immunology. 1982 Apr;45(4):621-8.
Resident mouse peritoneal macrophages (M phi) produced significant amounts of superoxide anion (O2-) in response to phagocytic stimuli. When M phi were exposed in vitro for 20 hr to fibroblast interferon (IFN-beta), their capacity to release O2- was significantly reduced, such reduction being more evident with increasing IFN-beta concentrations. In contrast, O2- production by M phi exposed for 20 hr to the lymphokine macrophage activating factor (MAF) or treated with either MAF or IFN-beta for 4 hr was not significantly different from that of control cells. This pattern of activity closely followed that of M phi-mediated suppression of lymphocyte proliferation, which was dramatically reduced by 20 hr exposure of M phi to IFN-beta, but unchanged by treatment with MAF. No correlation was however found between superoxide anion generation and enhancement of tumoricidal capacity in IFN-beta-treated M phi. We thus concluded that O2- does not play a relevant role in IFN-beta-induced M phi cytolysis, whereas the reduction of O2- production could be of major importance in the decrease of M phi suppression induced by IFN-beta.
驻留小鼠腹腔巨噬细胞（M phi）在吞噬刺激下会产生大量超氧阴离子（O2-）。当M phi在体外暴露于成纤维细胞干扰素（IFN-β）20小时后，其释放O2-的能力显著降低，且随着IFN-β浓度的增加，这种降低更为明显。相比之下，暴露于淋巴因子巨噬细胞活化因子（MAF）20小时或用MAF或IFN-β处理4小时的M phi产生的O2-与对照细胞无显著差异。这种活性模式与M phi介导的淋巴细胞增殖抑制密切相关，M phi暴露于IFN-β20小时会显著降低淋巴细胞增殖抑制，而用MAF处理则无变化。然而，在IFN-β处理的M phi中，超氧阴离子生成与杀肿瘤能力增强之间未发现相关性。因此，我们得出结论，O2-在IFN-β诱导的M phi细胞溶解中不起相关作用，而O2-产生的减少可能在IFN-β诱导的M phi抑制降低中起重要作用。
