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Journal of Virology, November 2007, p. 12525-12534, Vol. 81, No. 22
0022-538X/07/$08.00+0     doi:10.1128/JVI.00839-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Influenza Virus-Induced Type I Interferon Leads to Polyclonal B-Cell Activation but Does Not Break Down B-Cell Tolerance{triangledown}

Anne Woods,1 Fanny Monneaux,2 Pauline Soulas-Sprauel,1 Sylviane Muller,2 Thierry Martin,1 Anne-Sophie Korganow,1 and Jean-Louis Pasquali1*

INSERM U737, Université Louis Pasteur, Hôpitaux universitaires de Strasbourg, Strasbourg, France,1 CNRS UPR 9021, Institut de Biologie cellulaire et moléculaire, Strasbourg, France2

Received 19 April 2007/ Accepted 4 September 2007

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)F1] 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)F1 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.

* Corresponding author. Mailing address: INSERM U737, Université Louis Pasteur, Hôpitaux universitaires de Strasbourg, Strasbourg, France. Phone: 33 (0)3 90 24 39 83. Fax: 33 (0)3 90 24 40 16. E-mail: jean-louis.pasquali{at}hemato-ulp.u-strasbg.fr

{triangledown} Published ahead of print on 12 September 2007.

Journal of Virology, November 2007, p. 12525-12534, Vol. 81, No. 22
0022-538X/07/$08.00+0     doi:10.1128/JVI.00839-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Woods, A., Soulas-Sprauel, P., Jaulhac, B., Arditi, B., Knapp, A.-M., Pasquali, J.-L., Korganow, A.-S., Martin, T. (2008). MyD88 Negatively Controls Hypergammaglobulinemia with Autoantibody Production during Bacterial Infection. Infect. Immun. 76: 1657-1667 [Abstract] [Full Text]  


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