Please use this identifier to cite or link to this item: http://hdl.handle.net/1942/3929
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dc.contributor.authorCHOU, YK-
dc.contributor.authorHENDERIKX, P-
dc.contributor.authorVAINIENE, M-
dc.contributor.authorWHITHAM, R-
dc.contributor.authorBOURDETTE, D-
dc.contributor.authorCHOU, CHJ-
dc.contributor.authorHASHIM, G-
dc.contributor.authorOFFNER, H-
dc.contributor.authorVANDENBARK, AA-
dc.date.accessioned2007-11-30T07:51:00Z-
dc.date.available2007-11-30T07:51:00Z-
dc.date.issued1991-
dc.identifier.citationJOURNAL OF NEUROSCIENCE RESEARCH, 28(2). p. 280-290-
dc.identifier.issn0360-4012-
dc.identifier.urihttp://hdl.handle.net/1942/3929-
dc.description.abstractSeveral recently discovered lines of evidence support the involvement of myelin basic protein (BP)-specific T cells in multiple sclerosis (MS). To identify potentially relevant immunodominant T cell epitopes, human BP (Hu-BP)-reactive T cell lines were selected from MS and normal donors and tested for reactivity to cleavage fragments and synthetic peptides of Hu-BP. The MS T cell lines responded to more Hu-BP epitopes than did normal lines, showing biased recognition of the N terminal half of the molecule, and one region in the C terminal half, suggesting increased sensitization to BP. The MS lines also differed from normal lines in their decreased percentage of CD8+ T cells. One hundred nine T cell clones isolated from these lines confirmed the reactivity pattern of the lines but did not reflect the mixed phenotype, since all but three clones tested were CD4+. T cell clones from HLA-DR2 homozygous donors responded to a variety of epitopes, indicating that this molecule was permissive in its ability to restrict T cell responses. Other epitopes, including the immunodominant 149-170 sequence, were restricted by several different major histocompatibility complex (MHC) molecules from both MS and normal donors. T cell receptor (TCR) V gene products could be identified on six of 38 clones tested using monoclonal antibodies. From one HLA-DR2 homozygous donor, four of eight clones utilized V-beta-5.2 in response to different BP epitopes, providing initial support for the preferential use of a limited set of V region genes in the human response to BP. Preferential TCR V gene use in MS patients would provide the rationale to regulate selectively BP-reactive T cells through immunity directed at the TCR and thus test for the first time the hypothesis that BP-reactive T cells play a critical role in the pathogenesis of MS.-
dc.language.isoen-
dc.publisherWILEY-LISS-
dc.subject.otherMULTIPLE SCLEROSIS; V-REGION GENES; T-CELL RECEPTOR-
dc.titleSPECIFICITY OF HUMAN T-CELL CLONES REACTIVE TO IMMUNODOMINANT EPITOPES OF MYELIN BASIC-PROTEIN-
dc.typeJournal Contribution-
dc.identifier.epage290-
dc.identifier.issue2-
dc.identifier.spage280-
dc.identifier.volume28-
local.format.pages11-
dc.description.notesOREGON HLTH SCI UNIV,DEPT NEUROL,PORTLAND,OR 97201. OREGON HLTH SCI UNIV,DEPT MICROBIOL & IMMUNOL,PORTLAND,OR 97201. DR L WILLEMS INST,DEPT IMMUNOL,DIEPENBEEK,BELGIUM. INST PSYCHIAT & NEUROL,WARSAW,POLAND. COLUMBIA UNIV,NEW YORK,NY 10027. EMORY UNIV,DEPT NEUROL,ATLANTA,GA 30322. ST LUKES ROOSEVELT HOSP,DEPT MICROBIOL & SURG,NEW YORK,NY 10025.CHOU, YK, OREGON HLTH SCI UNIV,VET AFFAIRS MED CTR,DEPT NEUROIMMUNOL RES,151D,PORTLAND,OR 97201.-
local.type.refereedRefereed-
dc.bibliographicCitation.oldjcatA1-
dc.identifier.doi10.1002/jnr.490280215-
dc.identifier.isiA1991FA37700014-
dc.identifier.urlhttps://doi.org/10.1002/jnr.490280215-
item.fulltextNo Fulltext-
item.accessRightsClosed Access-
item.fullcitationCHOU, YK; HENDERIKX, P; VAINIENE, M; WHITHAM, R; BOURDETTE, D; CHOU, CHJ; HASHIM, G; OFFNER, H & VANDENBARK, AA (1991) SPECIFICITY OF HUMAN T-CELL CLONES REACTIVE TO IMMUNODOMINANT EPITOPES OF MYELIN BASIC-PROTEIN. In: JOURNAL OF NEUROSCIENCE RESEARCH, 28(2). p. 280-290.-
item.contributorCHOU, CHJ-
item.contributorVANDENBARK, AA-
item.contributorOFFNER, H-
item.contributorBOURDETTE, D-
item.contributorHENDERIKX, P-
item.contributorVAINIENE, M-
item.contributorHASHIM, G-
item.contributorWHITHAM, R-
item.contributorCHOU, YK-
crisitem.journal.issn0360-4012-
crisitem.journal.eissn1097-4547-
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