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Lymphocyte function—associated antigen 1 overexpression and t cell autoreactivity

dc.contributor.authorRichardson, Bruce C.en_US
dc.contributor.authorO'Rourke, Kenneth S.en_US
dc.date.accessioned2006-04-28T16:25:18Z
dc.date.available2006-04-28T16:25:18Z
dc.date.issued1994-08en_US
dc.identifier.citationRichardson, Bruce; O'Rourke, Kenneth (1994)."Lymphocyte function—associated antigen 1 overexpression and t cell autoreactivity." Arthritis & Rheumatism 37(9): 1363-1372. <http://hdl.handle.net/2027.42/37802>en_US
dc.identifier.issn0004-3591en_US
dc.identifier.issn1529-0131en_US
dc.identifier.urihttps://hdl.handle.net/2027.42/37802
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=7524510&dopt=citationen_US
dc.description.abstractObjective . To determine if DNA methylation inhibitors make T cells autoreactive by inducing lymphocyte function—associated antigen type 1 (LFA–1) (CD11a/CD18) overexpression. Methods . T cell clones were treated with 3 distinct DNA methylation inhibitors or were stably transfected with a CD18 cDNA in a mammalian expression vector, and the effects on LFA–1 expression and activation requirements were examined. Results . LFA–1 overexpression, caused by DNA methylation inhibitors or by transfection, correlates with the development of autoreactivity. Conclusion . LFA–1 overexpression may contribute to T cell autoreactivity.en_US
dc.format.extent989386 bytes
dc.format.extent3118 bytes
dc.format.mimetypeapplication/pdf
dc.format.mimetypetext/plain
dc.language.isoen_US
dc.publisherJohn Wiley & Sons, Inc.en_US
dc.subject.otherLife and Medical Sciencesen_US
dc.subject.otherRheumatologyen_US
dc.titleLymphocyte function—associated antigen 1 overexpression and t cell autoreactivityen_US
dc.typeArticleen_US
dc.rights.robotsIndexNoFollowen_US
dc.subject.hlbsecondlevelGeriatricsen_US
dc.subject.hlbtoplevelHealth Sciencesen_US
dc.description.peerreviewedPeer Revieweden_US
dc.contributor.affiliationumUniversity of Michigan, Ann Arbor, and the Ann Arbor Veterans Administration Hospital ; R4540 Kresge 1, Ann Arbor, MI 48109–0531en_US
dc.contributor.affiliationotherBowman Gray School of Medicine, Winston–Salem, North Carolinaen_US
dc.identifier.pmid7524510en_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/37802/1/1780370915_ftp.pdfen_US
dc.identifier.doihttp://dx.doi.org/10.1002/art.1780370915en_US
dc.identifier.sourceArthritis & Rheumatismen_US
dc.owningcollnameInterdisciplinary and Peer-Reviewed


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