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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
9
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pubmed:dateCreated |
1990-11-21
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pubmed:abstractText |
We have examined the expression of TCR genes in 4-hydroxy-3-nitrophenyl-acetyl (NP)-specific Ts cell hybridomas. Each of three independently isolated hybridomas expressed in-frame TCR alpha-chain rearrangements derived from the original suppressor Ts cell. Different V alpha and J alpha gene segments were rearranged and expressed in each Ts cell line. The only TCR beta-chain expressed in these cells was derived from the BW5147 fusion partner. Expression of the BW5147 beta-chain was found to correlate with cell surface Ag binding, inasmuch as subclones derived from one of the original Ts lines expressed greatly reduced levels of beta-chain mRNA and no longer bound to NP-coupled RBC. Subclones that continued to express beta-chain mRNA did bind to NP-coupled RBC. This suggests that the Ag receptor on Ts hybridomas is a TCR-alpha beta dimer composed of a unique alpha-chain and the BW5147 beta-chain. Ag binding could be modulated by preincubation of Ts hybridoma cells with anti-TCR-alpha beta antibody, thereby supporting this conclusion. Suppressor factor activity was measured in the conditioned media of Ts subclones that differed by 250-fold in levels of beta-chain mRNA expression. No difference in suppressor factor activity was found; conditioned media from these subclones suppressed both plaque-forming cell responses and delayed-type hypersensitivity responses at approximately equivalent dilutions. Suppressor factor activity in the conditioned media of both a beta-chain negative subclone and a beta-chain positive subclone could be absorbed with an antibody that recognizes the TCR alpha-chain, but not with an antibody that recognizes the TCR beta-chain. We conclude that suppressor factor activity in the conditioned media of these Ts hybridomas is not derived from surface TCR-alpha beta receptors, although it does share TCR alpha-chain determinants.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/DNA,
http://linkedlifedata.com/resource/pubmed/chemical/Oligonucleotides,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Antigen, T-Cell,
http://linkedlifedata.com/resource/pubmed/chemical/Suppressor Factors, Immunologic
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
0022-1767
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
145
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
2809-19
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:2170525-Amino Acid Sequence,
pubmed-meshheading:2170525-Animals,
pubmed-meshheading:2170525-Base Sequence,
pubmed-meshheading:2170525-Blotting, Northern,
pubmed-meshheading:2170525-Blotting, Southern,
pubmed-meshheading:2170525-Chromatography, Affinity,
pubmed-meshheading:2170525-Cloning, Molecular,
pubmed-meshheading:2170525-DNA,
pubmed-meshheading:2170525-Gene Rearrangement, alpha-Chain T-Cell Antigen Receptor,
pubmed-meshheading:2170525-Gene Rearrangement, beta-Chain T-Cell Antigen Receptor,
pubmed-meshheading:2170525-Gene Rearrangement, gamma-Chain T-Cell Antigen Receptor,
pubmed-meshheading:2170525-Hybridomas,
pubmed-meshheading:2170525-Immune Tolerance,
pubmed-meshheading:2170525-Mice,
pubmed-meshheading:2170525-Molecular Sequence Data,
pubmed-meshheading:2170525-Oligonucleotides,
pubmed-meshheading:2170525-Polymerase Chain Reaction,
pubmed-meshheading:2170525-RNA, Messenger,
pubmed-meshheading:2170525-Receptors, Antigen, T-Cell,
pubmed-meshheading:2170525-Suppressor Factors, Immunologic,
pubmed-meshheading:2170525-T-Lymphocytes, Regulatory
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pubmed:year |
1990
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pubmed:articleTitle |
Expression of functional alpha beta T cell receptor gene rearrangements in suppressor T cell hybridomas correlates with antigen binding, but not with suppressor cell function.
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pubmed:affiliation |
Genetics Institute, Cambridge, MA 02140.
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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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