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Influenza virus-induced type I interferon leads to polyclonal B-cell activation but does not break down B-cell tolerance.

Abstract : The link between infection and autoimmunity is not yet well understood. This study was designed to evaluate if an acute viral infection known to induce type I interferon production, like influenza, can by itself be responsible for the breakdown of immune tolerance and for autoimmunity. We first tested the effects of influenza virus on B cells in vitro. We then infected different transgenic mice expressing human rheumatoid factors (RF) in the absence or in the constitutive presence of the autoantigen (human immunoglobulin G [IgG]) and young lupus-prone mice [(NZB x NZW)F(1)] with influenza virus and looked for B-cell activation. In vitro, the virus induces B-cell activation through type I interferon production by non-B cells but does not directly stimulate purified B cells. In vivo, both RF and non-RF B cells were activated in an autoantigen-independent manner. This activation was abortive since IgM and IgM-RF production levels were not increased in infected mice compared to uninfected controls, whether or not anti-influenza virus human IgG was detected and even after viral rechallenge. As in RF transgenic mice, acute viral infection of (NZB x NZW)F(1) mice induced only an abortive activation of B cells and no increase in autoantibody production compared to uninfected animals. Taken together, these experiments show that virus-induced acute type I interferon production is not able by itself to break down B-cell tolerance in both normal and autoimmune genetic backgrounds.
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https://hal.archives-ouvertes.fr/hal-00284296
Contributor : Sylvie Pansiot <>
Submitted on : Monday, June 2, 2008 - 3:55:07 PM
Last modification on : Thursday, April 23, 2020 - 2:26:29 PM

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Anne Woods, Fanny Monneaux, Pauline Soulas-Sprauel, Sylviane Muller, Thierry Martin, et al.. Influenza virus-induced type I interferon leads to polyclonal B-cell activation but does not break down B-cell tolerance.. Journal of Virology, American Society for Microbiology, 2007, 81 (22), pp.12525-34. ⟨10.1128/JVI.00839-07⟩. ⟨hal-00284296⟩

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