Sharon N, Shoham J, Passwell J H
Samuel Jared Kushnick Pediatric Immunology Laboratory, Sheba Medical Centre, Sackler School of Medicine, Israel.
Int J Immunopharmacol. 1989;11(7):743-9. doi: 10.1016/0192-0561(89)90128-8.
Recombinant interferon preparations caused a dose-dependent increase of human monocyte cytotoxicity to the K562 and Daudi cell lines. Both rIFN-gamma and rIFN-beta enhanced this function to a similar extent, while rIFN-alpha c had less effect when compared on the basis of their anti-viral effects. Endotoxin and concanavalin A increased basal monocyte cytotoxicity while phagocytosis of latex particles had no effect. The increased monocyte cytotoxic effect of rIFN-beta was completely abrogated by monoclonal antibody to IFN-beta, while monoclonal antibody to IFN-gamma had no effect. However, monoclonal antibody to IFN-gamma only reduced the increased cytotoxic effect caused by rIFN-gamma by 25%. Catalase inhibited both basal monocyte cytotoxicity and the increase in cytotoxicity following addition of rIFN-gamma only slightly, suggesting that mechanisms other than the oxidative burst were active and could be induced by rIFN-gamma.
重组干扰素制剂可使人类单核细胞对K562和Daudi细胞系的细胞毒性呈剂量依赖性增加。rIFN-γ和rIFN-β对该功能的增强程度相似,而基于它们的抗病毒作用比较时,rIFN-αc的作用较小。内毒素和伴刀豆球蛋白A可增加基础单核细胞细胞毒性,而乳胶颗粒的吞噬作用则无影响。rIFN-β增强的单核细胞细胞毒性作用被抗IFN-β单克隆抗体完全消除,而抗IFN-γ单克隆抗体则无作用。然而,抗IFN-γ单克隆抗体仅使rIFN-γ引起的细胞毒性增加作用降低25%。过氧化氢酶仅轻微抑制基础单核细胞细胞毒性以及添加rIFN-γ后细胞毒性的增加,这表明除氧化爆发外的其他机制也起作用,且可被rIFN-γ诱导。