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<jats:title>ABSTRACT</jats:title> <jats:p>Interleukin-1α (IL-1α) and IL-1β are proinflammatory cytokines, which induce a plethora of genes and activities by binding to the type 1 IL-1 receptor (IL-1R1). We have investigated the role of IL-1 during pulmonary antiviral immune responses in IL-1R1<jats:sup>−/−</jats:sup> mice infected with influenza virus. IL-1R1<jats:sup>−/−</jats:sup> mice showed markedly reduced inflammatory pathology in the lung, primarily due to impaired neutrophil recruitment. Activation of CD4<jats:sup>+</jats:sup> T cells in secondary lymphoid organs and subsequent migration to the lung were impaired in the absence of IL-1R1. In contrast, activation of virus-specific cytotoxic T lymphocytes and killing of virus-infected cells in the lung were intact. Influenza virus-specific immunoglobulin G (IgG) and IgA antibody responses were intact, while the IgM response was markedly reduced in both serum and mucosal sites in IL-1R1<jats:sup>−/−</jats:sup> mice. We found significantly increased mortality in the absence of IL-1R1; however, lung viral titers were only moderately increased. Our results demonstrate that IL-1α/β mediate acute pulmonary inflammatory pathology while enhancing survival during influenza virus infection. IL-1α/β appear not to influence killing of virus-infected cells but to enhance IgM antibody responses and recruitment of CD4<jats:sup>+</jats:sup> T cells to the site of infection.</jats:p>

Original publication

DOI

10.1128/jvi.79.10.6441-6448.2005

Type

Journal article

Journal

Journal of Virology

Publisher

American Society for Microbiology

Publication Date

15/05/2005

Volume

79

Pages

6441 - 6448