Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 1990 Feb;85(2):563-9.
doi: 10.1172/JCI114473.

Regulation of macrophage function by interferon-gamma. Somatic cell genetic approaches in murine macrophage cell lines to mechanisms of growth inhibition, the oxidative burst, and expression of the chronic granulomatous disease gene

Affiliations

Regulation of macrophage function by interferon-gamma. Somatic cell genetic approaches in murine macrophage cell lines to mechanisms of growth inhibition, the oxidative burst, and expression of the chronic granulomatous disease gene

M Goldberg et al. J Clin Invest. 1990 Feb.

Erratum in

  • J Clin Invest 1990 Jun;85(6):2029

Abstract

The importance of oxidative cytocidal mechanisms of phagocytic cells in immune protection against microbial pathogens is uniquely revealed by chronic granulomatous disease (CGD), a genetic deficiency disease of man. This cytocidal response in mononuclear phagocytes is principally regulated by IFN-gamma. A somatic cell genetic approach was taken to select oxidative variants from a cloned murine macrophage cell line, J774.16, which formally permitted us to dissociate three regulatory effects of IFN-gamma on these cells: the antiproliferative effect, the antiviral effect, and production of superoxide anion. Half of the variants defective in O-2 production after phorbol myristate acetate stimulation were also resistant to the antiproliferative effects of IFN-gamma. This result suggests that IFN-gamma-induced growth inhibition and production of cytocidal oxygen intermediates are mediated via a common pathway. The somatic cell genetic approach has allowed us to develop in vitro macrophage models for several forms of CGD. One variant characterized in detail, D9, was unable to produce superoxide after stimulation by phorbol esters. At the molecular level, Northern blot analysis revealed that the mRNA encoding the large subunit of the putative CGD gene product, cytochrome b558, was absent in this variant. Another class of variants constitutively unable to produce O-2 or the cytochrome b558 mRNA could be induced to do so by IFN-gamma. These somatic mutants may be useful models in clarifying the role of the CGD gene product and its regulation in the production of cytocidal oxygen intermediates.

PubMed Disclaimer

Similar articles

Cited by

References

    1. J Clin Invest. 1967 Sep;46(9):1422-32 - PubMed
    1. J Immunol. 1984 Dec;133(6):3006-9 - PubMed
    1. J Exp Med. 1980 Oct 1;152(4):808-22 - PubMed
    1. J Exp Med. 1982 Dec 1;156(6):1780-93 - PubMed
    1. N Engl J Med. 1983 Feb 3;308(5):245-51 - PubMed

Publication types