Source:http://linkedlifedata.com/resource/pubmed/id/12671739
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
12
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pubmed:dateCreated |
2003-4-2
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pubmed:databankReference | |
pubmed:abstractText |
Defects in natural killer T (NK T) cell function and of interleukin-4 -production in SJL and NOD mice have been linked to susceptibility to autoimmune disease. As SJL and NOD mice both carry the T-cell receptor (TCR) alpha-chain locus "c" (Tcra(c)) haplotype, found in few other strains, we have attempted to determine the influence of Tcra polymorphism on NK T-cell recognition of ligand, selection, and immune responses. The majority of NK T cells use an "invariant" TRAV11J15 (previously called AV14J18 or Valpha14 Jalpha281) alpha- chain paired with either TRBV13-2, BV29, or BV1 to recognize ligands presented by mCD1 molecules, including the glycolipid alpha-galactosylceramide (alpha-GalCer). Sequencing of TRAV11 from the mouse strains B10.A (encoding the Tcra(b) haplotype), B10.A- Tcra(c), and NOD (Tcra(c)) shows that Tcra(c) has a single TRAV11 gene (TRAV11*01) and that Tcra(b) has a single expressed gene (TRAV11*02), plus a closely related pseudogene. There is no apparent difference in alpha-chain J-region usage or in the CDR3alpha sequence at the TRAV11-J15 junction between the haplotypes in TRAV11-bearing NK T cells. Using Biacore and tetramer-binding and decay assays, we have determined that the interaction between Tcra(c) TRAV11*01 NK T TCR and the mCD1/alpha-GalCer complex is slightly weaker than that of Tcra(b) (i.e., TRAV11*02) NK T TCR. These differences are minor compared with differences between agonist and antagonist ligands in other TCR systems, suggesting that it is unlikely that TCR polymorphism explains the defect in NK T cells in the autoimmune mouse strains.
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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 |
Mar
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pubmed:issn |
0093-7711
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
54
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
874-83
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:12671739-Amino Acid Sequence,
pubmed-meshheading:12671739-Animals,
pubmed-meshheading:12671739-Animals, Congenic,
pubmed-meshheading:12671739-Antigens, CD1,
pubmed-meshheading:12671739-Base Sequence,
pubmed-meshheading:12671739-DNA,
pubmed-meshheading:12671739-Galactosylceramides,
pubmed-meshheading:12671739-Genes, T-Cell Receptor alpha,
pubmed-meshheading:12671739-Haplotypes,
pubmed-meshheading:12671739-Killer Cells, Natural,
pubmed-meshheading:12671739-Kinetics,
pubmed-meshheading:12671739-Mice,
pubmed-meshheading:12671739-Mice, Inbred C57BL,
pubmed-meshheading:12671739-Mice, Inbred NOD,
pubmed-meshheading:12671739-Molecular Sequence Data,
pubmed-meshheading:12671739-Polymorphism, Genetic,
pubmed-meshheading:12671739-Receptors, Antigen, T-Cell, alpha-beta,
pubmed-meshheading:12671739-Sequence Homology, Amino Acid,
pubmed-meshheading:12671739-Sequence Homology, Nucleic Acid,
pubmed-meshheading:12671739-T-Lymphocyte Subsets
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pubmed:year |
2003
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pubmed:articleTitle |
Surprisingly minor influence of TRAV11 (Valpha14) polymorphism on NK T-receptor mCD1/alpha-galactosylceramide binding kinetics.
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pubmed:affiliation |
IMM1, Department of Immunology, The Scripps Research Institute, La Jolla, CA 92037, 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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