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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
1992-8-7
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pubmed:abstractText |
The restricted usage of particular T cell receptor beta chain genes in autoimmune disease was studied in LEW rats using T cell hybridomas specific for an immunodominant sequence of bovine retinal S-Ag, which induces experimental autoimmune uveoretinitis. T cell hybridomas from a pathogenic T cell line, R858, specific for residues 273-289 of bovine retinal S-Ag were analyzed in order to determine the contribution of their TCR V beta to self specificity as determined by recognition of the pathogenic epitope represented in the autologous rat S-Ag sequence. Six different, functional TCR rearrangements were expressed by the panel of hybridomas, including two distinct V beta 8.2 rearrangements and functional V beta 10, V beta 14, V beta 19 rearrangements, and an unidentified V beta gene. All hybridomas were Ag specific and reacted both to nonself-peptide derivatives as well as to self-peptide homologues. No unique pattern of peptide reactivity distinguished V beta 8.2+ hybridomas from V beta 8.2- hybridomas; all of the hybridomas were most reactive to the nonself sequences and reacted to self peptide with one to three orders of magnitude less sensitivity. However, all V beta 8.2+ hybridomas were much better responders overall and were activated by lower concentrations of all peptides than were V beta 8.2- hybridomas. Although V beta 8.2 gene usage is strongly associated with autoimmune pathology, these data show that in LEW rats several different TCR V beta genes are utilized in response to a short pathogenic sequence of this autoantigen and show that V beta 8.2 receptors are not uniquely self-reactive. However, the enhanced reactivity to Ag of V beta 8.2+ hybridomas relative to V beta 8.2- hybridomas specific for the same peptide may help explain the close association of V beta 8.2 TCR gene usage with pathogenicity found in autoimmune disease models.
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pubmed:grant | |
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 |
Jul
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pubmed:issn |
0008-8749
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
142
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
275-86
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:1320462-Amino Acid Sequence,
pubmed-meshheading:1320462-Animals,
pubmed-meshheading:1320462-Antigens, CD4,
pubmed-meshheading:1320462-Autoantigens,
pubmed-meshheading:1320462-Autoimmune Diseases,
pubmed-meshheading:1320462-Base Sequence,
pubmed-meshheading:1320462-Disease Models, Animal,
pubmed-meshheading:1320462-Female,
pubmed-meshheading:1320462-Gene Rearrangement, beta-Chain T-Cell Antigen Receptor,
pubmed-meshheading:1320462-Hybridomas,
pubmed-meshheading:1320462-Interleukin-2,
pubmed-meshheading:1320462-Molecular Sequence Data,
pubmed-meshheading:1320462-Rats,
pubmed-meshheading:1320462-Rats, Inbred Lew,
pubmed-meshheading:1320462-Receptors, Antigen, T-Cell, alpha-beta,
pubmed-meshheading:1320462-Uveitis, Posterior
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pubmed:year |
1992
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pubmed:articleTitle |
Multiple, autoreactive TCR V beta genes utilized in response to a small pathogenic peptide of an autoantigen in EAU.
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pubmed:affiliation |
Department of Microbiology, University of Minnesota, Minneapolis 55455.
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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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