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A role for calreticulin in the pathogenesis of rheumatoid arthritis

dc.contributor.authorHoloshitz, Josephen_US
dc.contributor.authorDe Almeida, Denise E.en_US
dc.contributor.authorLing, Songen_US
dc.date.accessioned2011-01-31T17:57:35Z
dc.date.available2011-12-02T15:41:52Zen_US
dc.date.issued2010-10en_US
dc.identifier.citationHoloshitz, Joseph; De Almeida, Denise E.; Ling, Song; (2010). "A role for calreticulin in the pathogenesis of rheumatoid arthritis." Annals of the New York Academy of Sciences 1209(1 Clearance of Dying Cells in Healthy and Diseased Immune Systems ): 91-98. <http://hdl.handle.net/2027.42/79357>en_US
dc.identifier.issn0077-8923en_US
dc.identifier.issn1749-6632en_US
dc.identifier.urihttps://hdl.handle.net/2027.42/79357
dc.description.abstractCalreticulin (CRT) plays a role in the clearance of dying cells and has been implicated in autoimmunity. Recent evidence indicates that cell surface CRT (csCRT) acts as a signal transducing receptor for the rheumatoid arthritis (RA) shared epitope (SE). The SE binding site on CRT has been mapped to amino acid residues 217–223 in the P-domain. Upon interaction with dendritic cells (DCs), the SE activates potent immune regulatory events. In CD8α + DCs, which express higher abundance of csCRT, the SE inhibits the tolerogenic enzyme indoleamine 2,3 dioxygenase with resultant inhibition of regulatory T (Treg) cell differentiation. In CD8α − DCs, the SE ligand increases secretion of IL-6 and IL-23 and facilitates generation of Th17 cells, a T cell subset known to play a role in autoimmunity. On the basis of these recent findings, we discuss the possibility that the csCRT may play a pathogenic role in RA by transducing SE-activated Th17-polarizing signals.en_US
dc.format.extent348961 bytes
dc.format.extent3106 bytes
dc.format.mimetypeapplication/pdf
dc.format.mimetypetext/plain
dc.publisherBlackwell Publishing Incen_US
dc.subject.otherCalreticulinen_US
dc.subject.otherRheumatoid Arthritisen_US
dc.subject.otherShared Epitopeen_US
dc.subject.otherNitric Oxideen_US
dc.subject.otherTh17en_US
dc.subject.otherTregen_US
dc.titleA role for calreticulin in the pathogenesis of rheumatoid arthritisen_US
dc.typeArticleen_US
dc.rights.robotsIndexNoFollowen_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 Medical Center, Ann Arbor, Michiganen_US
dc.identifier.pmid20958321en_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/79357/1/j.1749-6632.2010.05745.x.pdf
dc.identifier.doi10.1111/j.1749-6632.2010.05745.xen_US
dc.identifier.sourceAnnals of the New York Academy of Sciencesen_US
dc.owningcollnameInterdisciplinary and Peer-Reviewed


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