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.