Publications
2007
Woods Anne, Monneaux Fanny, Soulas-Sprauel Pauline, Muller Sylviane, Martin Thierry, Korganow Anne-Sophie, Pasquali Jean-Louis
Influenza virus-induced type I interferon leads to polyclonal B-cell activation but does not break down B-cell tolerance Article de journal
Dans: Journal of Virology, vol. 81, no. 22, p. 12525–12534, 2007, ISSN: 0022-538X.
Résumé | Liens | BibTeX | Étiquettes: Animals, Antibody Formation, Autoantibodies, Autoantigens, Autoimmunity, B-Lymphocytes, Humans, I2CT, Immune Tolerance, Immunoglobulin M, Inbred Strains, Influenza A virus, Interferon Type I, Lymphocyte Activation, Mice, Monneaux, Rheumatoid Factor, Team-Dumortier, transgenic
@article{woods_influenza_2007,
title = {Influenza virus-induced type I interferon leads to polyclonal B-cell activation but does not break down B-cell tolerance},
author = {Anne Woods and Fanny Monneaux and Pauline Soulas-Sprauel and Sylviane Muller and Thierry Martin and Anne-Sophie Korganow and Jean-Louis Pasquali},
doi = {10.1128/JVI.00839-07},
issn = {0022-538X},
year = {2007},
date = {2007-01-01},
journal = {Journal of Virology},
volume = {81},
number = {22},
pages = {12525--12534},
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.},
keywords = {Animals, Antibody Formation, Autoantibodies, Autoantigens, Autoimmunity, B-Lymphocytes, Humans, I2CT, Immune Tolerance, Immunoglobulin M, Inbred Strains, Influenza A virus, Interferon Type I, Lymphocyte Activation, Mice, Monneaux, Rheumatoid Factor, Team-Dumortier, transgenic},
pubstate = {published},
tppubtype = {article}
}
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.