tetano
Editor, Senior Moderator
J Innate Immun. 2014 Jan 10. [Epub ahead of print]
Type I Interferon Plays Opposing Roles in Cytotoxicity and Interferon-γ Production by Natural Killer and CD8 T Cells after Influenza A Virus Infection in Mice.
Arimori Y, Nakamura R, Yamada H, Shibata K, Maeda N, Kase T, Yoshikai Y.
Author information
Abstract
Type I interferons (IFNs) promote natural killer (NK) and CD8+ T-cell responses, which play a role not only in the resolution of infection but also in the induction of acute lung injury following influenza A virus infection. We show here that IFN-α receptor knock-out (Ifnar1-/-) mice exhibited impaired cytotoxic activity as well as an increased ability of NK and CD8+ T cells to produce IFN-γ after infection with influenza virus A/FM/1/47 (H1N1, a mouse-adapted strain). A deficiency in IFNAR signaling significantly impaired IL-10 production in influenza virus-infected lungs and enhanced IFN-γ production by NK cells, which were suppressed by exogenous IL-10. Depletion of NK cells but not CD8+ T cells in Ifnar1-/- mice improved the survival rate after A/FM/1/47 infection, indicating that NK cells are responsible for acute lung injury in Ifnar1-/- mice following influenza A virus infection, although the depletion of IFN-γ did not improve the outcome. Thus, type I IFN signaling plays a role not only in the upregulation of cytotoxicity but also in the downregulation of some effector mechanisms including IFN-γ production by NK and CD8+ T cells via IL-10 production. ? 2014 S. Karger AG, Basel.
PMID:
24435166
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/24435166
Type I Interferon Plays Opposing Roles in Cytotoxicity and Interferon-γ Production by Natural Killer and CD8 T Cells after Influenza A Virus Infection in Mice.
Arimori Y, Nakamura R, Yamada H, Shibata K, Maeda N, Kase T, Yoshikai Y.
Author information
Abstract
Type I interferons (IFNs) promote natural killer (NK) and CD8+ T-cell responses, which play a role not only in the resolution of infection but also in the induction of acute lung injury following influenza A virus infection. We show here that IFN-α receptor knock-out (Ifnar1-/-) mice exhibited impaired cytotoxic activity as well as an increased ability of NK and CD8+ T cells to produce IFN-γ after infection with influenza virus A/FM/1/47 (H1N1, a mouse-adapted strain). A deficiency in IFNAR signaling significantly impaired IL-10 production in influenza virus-infected lungs and enhanced IFN-γ production by NK cells, which were suppressed by exogenous IL-10. Depletion of NK cells but not CD8+ T cells in Ifnar1-/- mice improved the survival rate after A/FM/1/47 infection, indicating that NK cells are responsible for acute lung injury in Ifnar1-/- mice following influenza A virus infection, although the depletion of IFN-γ did not improve the outcome. Thus, type I IFN signaling plays a role not only in the upregulation of cytotoxicity but also in the downregulation of some effector mechanisms including IFN-γ production by NK and CD8+ T cells via IL-10 production. ? 2014 S. Karger AG, Basel.
PMID:
24435166
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/24435166