信使核糖核酸
CD64
反转运蛋白
单核细胞
分子生物学
受体
干扰素γ
呼吸爆发
干扰素
化学
Fc受体
生物
免疫系统
免疫学
生物化学
基因
膜
作者
Marco A. Cassatella,Rebecca M. Flynn,Miguel Aste Amezaga,Flavia Bazzoni,Federica Vicentini,Giorgio Trinchieri
标识
DOI:10.1016/0006-291x(90)92131-i
摘要
Immune interferon (IFN-γ) induces in human neutrophils accumulation of the mRNA for the high affinity receptor for monomeric IgG (FcγR-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 FcγR-I mRNA by IFN-γ, without requirement of protein synthesis. Unlike what is observed in neutrophils, induction by IFN-γ of macrophage FcγR-I mRNA was significantly depressed by the Na+H+ antiporter inhibitor amiloride. These results indicate that phagocytes' FcγR-I mRNA induction by IFN-γ is regulated by different mechanisms depending on the target cells.
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