rdf:type |
|
lifeskim:mentions |
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pubmed:issue |
22
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pubmed:dateCreated |
2007-10-29
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pubmed:abstractText |
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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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/17855528-10426316,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17855528-10657630,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17855528-10915562,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/17855528-9198668
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pubmed:language |
eng
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pubmed:journal |
|
pubmed:citationSubset |
IM
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pubmed:chemical |
|
pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
0022-538X
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pubmed:author |
|
pubmed:issnType |
Print
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pubmed:volume |
81
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pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
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pubmed:pagination |
12525-34
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:17855528-Animals,
pubmed-meshheading:17855528-Antibody Formation,
pubmed-meshheading:17855528-Autoantibodies,
pubmed-meshheading:17855528-Autoantigens,
pubmed-meshheading:17855528-Autoimmunity,
pubmed-meshheading:17855528-B-Lymphocytes,
pubmed-meshheading:17855528-Humans,
pubmed-meshheading:17855528-Immune Tolerance,
pubmed-meshheading:17855528-Immunoglobulin M,
pubmed-meshheading:17855528-Influenza A virus,
pubmed-meshheading:17855528-Interferon Type I,
pubmed-meshheading:17855528-Lymphocyte Activation,
pubmed-meshheading:17855528-Mice,
pubmed-meshheading:17855528-Mice, Inbred Strains,
pubmed-meshheading:17855528-Mice, Transgenic,
pubmed-meshheading:17855528-Rheumatoid Factor
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pubmed:year |
2007
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pubmed:articleTitle |
Influenza virus-induced type I interferon leads to polyclonal B-cell activation but does not break down B-cell tolerance.
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pubmed:affiliation |
INSERM U737, Université Louis Pasteur, Hôpitaux universitaires de Strasbourg, Strasbourg, France.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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