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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
1
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pubmed:dateCreated |
2004-1-6
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pubmed:abstractText |
Type I and II interferons (IFNs) exert opposing effects on the progression of multiple sclerosis, even though both IFNs use the signal transducer and activator of transcription 1 (STAT1) as a signaling mediator. Here we report that STAT1-deficient mice expressing a transgenic T cell receptor against myelin basic protein spontaneously develop experimental autoimmune encephalomyelitis with dramatically increased frequency. The heightened susceptibility to this autoimmune disease appears to be triggered by a reduced number as well as a functional impairment of the CD4+ CD25+ regulatory T cells in STAT1-deficient animals. Adoptive transfer of wild-type regulatory T cells into STAT1-deficient hosts is sufficient to prevent the development of autoimmune disease. These results demonstrate an essential role of STAT1 in the maintenance of immunological self-tolerance.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/14699080-10595504,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14699080-10605010,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14699080-10637555,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14699080-10640742,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14699080-10754318,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14699080-10795741,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14699080-10837065,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14699080-10850488,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14699080-10880533,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14699080-10917889,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14699080-11290338,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14699080-11390442,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14699080-11420036,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14699080-11505971,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14699080-11526392,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14699080-11722628,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14699080-11869690,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14699080-7520367,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14699080-7574495,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14699080-7636184,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14699080-7678116,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14699080-7679952,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14699080-7693454,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14699080-8608597,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14699080-8608598,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14699080-8616884,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14699080-8871615,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14699080-9374464,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14699080-9463404,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14699080-9492992,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14699080-9570536,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14699080-9620592,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14699080-9670041,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14699080-9815265
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
0022-1007
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
5
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pubmed:volume |
199
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
25-34
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pubmed:dateRevised |
2011-9-26
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pubmed:meshHeading |
pubmed-meshheading:14699080-Adoptive Transfer,
pubmed-meshheading:14699080-Animals,
pubmed-meshheading:14699080-Autoimmune Diseases,
pubmed-meshheading:14699080-CD4-Positive T-Lymphocytes,
pubmed-meshheading:14699080-DNA-Binding Proteins,
pubmed-meshheading:14699080-Disease Susceptibility,
pubmed-meshheading:14699080-Mice,
pubmed-meshheading:14699080-Mice, Knockout,
pubmed-meshheading:14699080-Mice, Transgenic,
pubmed-meshheading:14699080-Receptors, Antigen, T-Cell,
pubmed-meshheading:14699080-Receptors, Interleukin-2,
pubmed-meshheading:14699080-STAT1 Transcription Factor,
pubmed-meshheading:14699080-Signal Transduction,
pubmed-meshheading:14699080-T-Lymphocytes,
pubmed-meshheading:14699080-Trans-Activators
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pubmed:year |
2004
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pubmed:articleTitle |
Impaired development of CD4+ CD25+ regulatory T cells in the absence of STAT1: increased susceptibility to autoimmune disease.
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pubmed:affiliation |
Department of Biology, University of California San Diego, Bonner Hall 3138, 9500 Gilman Drive, La Jolla, CA 92093, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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