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
. 1993 Nov 1;178(5):1725-32.
doi: 10.1084/jem.178.5.1725.

Response to influenza infection in mice with a targeted disruption in the interferon gamma gene

Affiliations

Response to influenza infection in mice with a targeted disruption in the interferon gamma gene

M B Graham et al. J Exp Med. .

Abstract

Interferon gamma (IFN-gamma) is a pleiotropic cytokine secreted by T lymphocytes and natural killer (NK) cells and has been noted to be a first line of host defense in the control of viral infections. To examine further the role of this cytokine in the control of viral infections, mice with a targeted mutation in the IFN-gamma gene were infected with influenza virus, and the in vivo antibody and cell-mediated immune response to viral infection were examined. In addition, cell lines and clones were derived from the immunized animals and the in vitro cytokine production and cytotoxic T lymphocyte (CTL) response were analyzed. The absence of IFN-gamma led to increased production of influenza-specific IgG1, IL-4, and IL-5 as compared to wild-type littermate control animals. In contrast, there was no difference noted in the development of an effective CTL response between IFN-gamma-deficient and wild-type animals. In this model of experimental influenza infection, IFN-gamma is not necessary for the development of an effective humoral or cellular immune response to challenge with this respiratory virus.

PubMed Disclaimer

Similar articles

Cited by

References

    1. J Exp Med. 1982 Apr 1;155(4):1198-203 - PubMed
    1. Nature. 1982 Jan 14;295(5845):150-2 - PubMed
    1. Eur J Immunol. 1983 Sep;13(9):707-11 - PubMed
    1. J Exp Med. 1984 Sep 1;160(3):814-26 - PubMed
    1. J Immunol. 1985 Mar;134(3):1644-52 - PubMed

Publication types

MeSH terms