Source:http://linkedlifedata.com/resource/pubmed/id/18469818
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
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pubmed:dateCreated |
2008-5-20
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pubmed:abstractText |
The T cell antigen receptor (TCR)-CD3 complex is unique in having ten cytoplasmic immunoreceptor tyrosine-based activation motifs (ITAMs). The physiological importance of this high TCR ITAM number is unclear. Here we generated 25 groups of mice expressing various combinations of wild-type and mutant ITAMs in TCR-CD3 complexes. Mice with fewer than seven wild-type CD3 ITAMs developed a lethal, multiorgan autoimmune disease caused by a breakdown in central rather than peripheral tolerance. Although there was a linear correlation between the number of wild-type CD3 ITAMs and T cell proliferation, cytokine production was unaffected by ITAM number. Thus, high ITAM number provides scalable signaling that can modulate proliferation yet ensure effective negative selection and prevention of autoimmunity.
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pubmed:grant | |
pubmed:commentsCorrections | |
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 |
Jun
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pubmed:issn |
1529-2916
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pubmed:author |
pubmed-author:BaquetZacharyZ,
pubmed-author:BoydKelli LKL,
pubmed-author:ChruscinskiAndrzejA,
pubmed-author:EderKelly DurickKD,
pubmed-author:ForbesKarenK,
pubmed-author:HolstJeffJ,
pubmed-author:SinghHarvirH,
pubmed-author:SmeyneRichardR,
pubmed-author:UtzPaul JPJ,
pubmed-author:VignaliDario A ADA,
pubmed-author:WangHaopengH,
pubmed-author:WorkmanCreg JCJ,
pubmed-author:van OersNicolai S CNS
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pubmed:issnType |
Electronic
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pubmed:volume |
9
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
658-66
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pubmed:meshHeading | |
pubmed:year |
2008
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pubmed:articleTitle |
Scalable signaling mediated by T cell antigen receptor-CD3 ITAMs ensures effective negative selection and prevents autoimmunity.
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pubmed:affiliation |
Department of Immunology, St. Jude Children's Research Hospital, Memphis, Tennessee 38105-2794, USA.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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