Cassatella M A, Flynn R M, Amezaga M A, Bazzoni F, Vicentini F, Trinchieri G
Institute of General Pathology, University of Verona, Italy.
Biochem Biophys Res Commun. 1990 Jul 31;170(2):582-8. doi: 10.1016/0006-291x(90)92131-i.
Immune interferon (IFN-gamma) induces in human neutrophils accumulation of the mRNA for the high affinity receptor for monomeric IgG (Fc gamma R-I, CD64) with a mechanism that is independent from de novo protein synthesis and from activation of the Na+/H+ antiporter. Monocyte-derived macrophages can also be induced to express high levels of Fc gamma R-I mRNA by IFN-gamma, without requirement of protein synthesis. Unlike what is observed in neutrophils, induction by IFN-gamma of macrophage Fc gamma R-I mRNA was significantly depressed by the Na+/H+ antiporter inhibitor amiloride. These results indicate that phagocytes' Fc gamma R-I mRNA induction by IFN-gamma is regulated by different mechanisms depending on the target cells.
免疫干扰素（IFN-γ）可诱导人类中性粒细胞中单体IgG高亲和力受体（FcγR-I，CD64）的mRNA积累，其机制独立于从头蛋白质合成和Na+/H+反向转运体的激活。单核细胞衍生的巨噬细胞也可被IFN-γ诱导表达高水平的FcγR-I mRNA，且无需蛋白质合成。与在中性粒细胞中观察到的情况不同，Na+/H+反向转运体抑制剂阿米洛利可显著抑制IFN-γ对巨噬细胞FcγR-I mRNA的诱导。这些结果表明，IFN-γ对吞噬细胞FcγR-I mRNA的诱导因靶细胞而异，受不同机制调控。
