Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6415
pubmed:dateCreated
1993-4-6
pubmed:abstractText
Multiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system in which a restricted cellular immune response has been observed. In order to establish whether such T cell responses are likely to be antigen-specific particularly with regard to myelin basic protein (MBP), we analysed T-cell receptor (TCR) gene rearrangements directly from MS brain plaques, using the polymerase chain reaction on reverse transcribed messenger RNA, and compared these with TCR of previously described MBP-specific T cell clones from MS and the rat model experimental allergic encephalomyelitis. Rearranged V beta 5.2 genes were detected in the brains of all patients who were HLA DRB1*1501, DQA1*0102, DQB1*0602, DPB1*0401. The V beta 5.2-D beta-J beta sequences in these MS brain plaques revealed five motifs. One of the common motifs was identical to that described for the VDJ region of a V beta 5.2 T-cell clone. This clone was from an MS patient who was HLA DRB1*1501, DQB1*0602, DPB1*0401, and it was cytotoxic towards targets containing the MBP peptide 89-106 (ref. 1). The deduced amino-acid sequence of this VDJ rearrangement, Leu-Arg-Gly, has also been described in rat T cells cloned from experimental allergic encephalomyelitis lesions, which are specific for MBP peptide 87-99 (ref. 2). VDJ sequences with specificity for this MBP epitope constitute a large fraction (40%) of the TCR V beta 5.2 N(D)N rearrangements in MS lesions. The capacity of rat T cells with these VDJ sequences to cause experimental allergic encephalomyelitis and the prevalence of such sequences in demyelinated human lesions indicate that T cells with this rearranged TCR may be critical in MS.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0028-0836
pubmed:author
pubmed:issnType
Print
pubmed:day
4
pubmed:volume
362
pubmed:owner
NLM
pubmed:authorsComplete
N
pubmed:pagination
68-70
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:7680433-Amino Acid Sequence, pubmed-meshheading:7680433-Animals, pubmed-meshheading:7680433-Antigens, CD3, pubmed-meshheading:7680433-Base Sequence, pubmed-meshheading:7680433-Brain, pubmed-meshheading:7680433-Cloning, Molecular, pubmed-meshheading:7680433-Encephalomyelitis, Autoimmune, Experimental, pubmed-meshheading:7680433-Gene Rearrangement, beta-Chain T-Cell Antigen Receptor, pubmed-meshheading:7680433-HLA-D Antigens, pubmed-meshheading:7680433-Humans, pubmed-meshheading:7680433-Molecular Sequence Data, pubmed-meshheading:7680433-Multiple Sclerosis, pubmed-meshheading:7680433-Myelin Basic Proteins, pubmed-meshheading:7680433-Oligodeoxyribonucleotides, pubmed-meshheading:7680433-Phenotype, pubmed-meshheading:7680433-Polymerase Chain Reaction, pubmed-meshheading:7680433-RNA, Messenger, pubmed-meshheading:7680433-Rats, pubmed-meshheading:7680433-Spinal Cord, pubmed-meshheading:7680433-T-Lymphocytes
pubmed:year
1993
pubmed:articleTitle
Selection for T-cell receptor V beta-D beta-J beta gene rearrangements with specificity for a myelin basic protein peptide in brain lesions of multiple sclerosis.
pubmed:affiliation
Department of Neurology and Neurological Science, Stanford University School of Medicine, California 94305-5235.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't