Interferon gamma induces in human neutrophils and macrophages expression of the mRNA for the high affinity receptor for monomeric IgG (FcγR-I or CD64)

https://doi.org/10.1016/0006-291X(90)92131-IGet rights and content

Abstract

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.

References (20)

  • G. Trinchieri et al.

    Immunol. Today

    (1985)
  • P. Lengyel

    Meth. Enzymol

    (1981)
  • M.A. Cassatella et al.

    Biochem. Biophys. Res. Commun

    (1985)
  • G. Berton et al.

    Biochem. Biophys. Res. Commun

    (1986)
  • E.T. Dayton et al.

    Blood

    (1985)
  • C. Frelin et al.

    Kidney International

    (1987)
  • J. Weil et al.

    Nature (Lond.)

    (1983)
  • B. Perussia et al.

    J. Immunol

    (1987)
  • M.A. Cassatella et al.

    Immunology

    (1988)
  • B. Perussia et al.

    J. Exp. Med

    (1983)
There are more references available in the full text version of this article.

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