A role for calreticulin in the pathogenesis of rheumatoid arthritis
dc.contributor.author | Holoshitz, Joseph | en_US |
dc.contributor.author | De Almeida, Denise E. | en_US |
dc.contributor.author | Ling, Song | en_US |
dc.date.accessioned | 2011-01-31T17:57:35Z | |
dc.date.available | 2011-12-02T15:41:52Z | en_US |
dc.date.issued | 2010-10 | en_US |
dc.identifier.citation | Holoshitz, 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.issn | 0077-8923 | en_US |
dc.identifier.issn | 1749-6632 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/79357 | |
dc.description.abstract | Calreticulin (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.extent | 348961 bytes | |
dc.format.extent | 3106 bytes | |
dc.format.mimetype | application/pdf | |
dc.format.mimetype | text/plain | |
dc.publisher | Blackwell Publishing Inc | en_US |
dc.subject.other | Calreticulin | en_US |
dc.subject.other | Rheumatoid Arthritis | en_US |
dc.subject.other | Shared Epitope | en_US |
dc.subject.other | Nitric Oxide | en_US |
dc.subject.other | Th17 | en_US |
dc.subject.other | Treg | en_US |
dc.title | A role for calreticulin in the pathogenesis of rheumatoid arthritis | en_US |
dc.type | Article | en_US |
dc.rights.robots | IndexNoFollow | en_US |
dc.subject.hlbsecondlevel | Science (General) | en_US |
dc.subject.hlbtoplevel | Science | en_US |
dc.description.peerreviewed | Peer Reviewed | en_US |
dc.contributor.affiliationum | Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, Michigan | en_US |
dc.identifier.pmid | 20958321 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/79357/1/j.1749-6632.2010.05745.x.pdf | |
dc.identifier.doi | 10.1111/j.1749-6632.2010.05745.x | en_US |
dc.identifier.source | Annals of the New York Academy of Sciences | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
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