Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
2003-4-2
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.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0093-7711
pubmed:author
pubmed:issnType
Print
pubmed:volume
54
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
874-83
pubmed:dateRevised
2007-11-14
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
pubmed:year
2003
pubmed:articleTitle
Surprisingly minor influence of TRAV11 (Valpha14) polymorphism on NK T-receptor mCD1/alpha-galactosylceramide binding kinetics.
pubmed:affiliation
IMM1, Department of Immunology, The Scripps Research Institute, La Jolla, CA 92037, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't