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Nitric Oxide Signaling Triggered by the Rheumatoid Arthritis–Shared Epitope
dc.contributor.authorHoloshitz, Josephen_US
dc.contributor.authorLing, Songen_US
dc.date.accessioned2010-06-01T19:05:04Z
dc.date.available2010-06-01T19:05:04Z
dc.date.issued2007-09en_US
dc.identifier.citationHOLOSHITZ, JOSEPH; LING, SONG (2007). "Nitric Oxide Signaling Triggered by the Rheumatoid Arthritis–Shared Epitope." Annals of the New York Academy of Sciences 1110(1 Autoimmunity, Part B Novel Applications of Basic Research ): 73-83. <http://hdl.handle.net/2027.42/72272>en_US
dc.identifier.issn0077-8923en_US
dc.identifier.issn1749-6632en_US
dc.identifier.urihttps://hdl.handle.net/2027.42/72272
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=17911422&dopt=citationen_US
dc.description.abstractMany immune-mediated diseases are associated with particular MHC class I or class II alleles. In rheumatoid arthritis (RA-shared), the vast majority of patients possess HLA-DRB1 alleles encoding a shared epitope, which is a five–amino acid sequence motif in positions 70–74 of the HLA-DRΒ chain. The mechanistic basis for this association is unknown. Here we discuss recent evidence suggesting that the shared epitope may act as an allele-specific ligand that triggers increased nitric oxide (NO) production in opposite cells with resultant immune dysregulation. We propose that by doing that, the RA-shared shared epitope may form an unintended bridge between the innate and adaptive immune systems, thereby allowing aberrant signaling events that could trigger disease.en_US
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dc.format.extent3109 bytes
dc.format.mimetypeapplication/pdf
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dc.publisherBlackwell Publishing Incen_US
dc.rights2007 New York Academy of Sciencesen_US
dc.subject.otherAutoimmunityen_US
dc.subject.otherMHC–Disease Associationen_US
dc.subject.otherSignal Transductionen_US
dc.titleNitric Oxide Signaling Triggered by the Rheumatoid Arthritis–Shared Epitopeen_US
dc.typeArticleen_US
dc.subject.hlbsecondlevelScience (General)en_US
dc.subject.hlbtoplevelScienceen_US
dc.description.peerreviewedPeer Revieweden_US
dc.contributor.affiliationumDepartment of Internal Medicine, University of Michigan, Ann Arbor, Michigan, USAen_US
dc.identifier.pmid17911422en_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/72272/1/annals.1423.009.pdf
dc.identifier.doi10.1196/annals.1423.009en_US
dc.identifier.sourceAnnals of the New York Academy of Sciencesen_US
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dc.owningcollnameInterdisciplinary and Peer-Reviewed


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