Presentation of arthritogenic peptide to antigen-specific T cells by fibroblast-like synoviocytes
dc.contributor.author | Tran, Chinh Nguyen | en_US |
dc.contributor.author | Davis, Michael J. | en_US |
dc.contributor.author | Tesmer, Laura A. | en_US |
dc.contributor.author | Endres, Judith L. | en_US |
dc.contributor.author | Motyl, Christopher D. | en_US |
dc.contributor.author | Smuda, Craig | en_US |
dc.contributor.author | Somers, Emily C. | en_US |
dc.contributor.author | Chung, Kevin C. | en_US |
dc.contributor.author | Urquhart, Andrew G. | en_US |
dc.contributor.author | Lundy, Steven K. | en_US |
dc.contributor.author | Kovats, Susan | en_US |
dc.contributor.author | Fox, David A. | en_US |
dc.date.accessioned | 2007-09-20T18:36:52Z | |
dc.date.available | 2008-09-08T14:25:14Z | en_US |
dc.date.issued | 2007-05 | en_US |
dc.identifier.citation | Tran, Chinh N.; Davis, Michael J.; Tesmer, Laura A.; Endres, Judith L.; Motyl, Christopher D.; Smuda, Craig; Somers, Emily C.; Chung, Kevin C.; Urquhart, Andrew G.; Lundy, Steven K.; Kovats, Susan; Fox, David A. (2007)."Presentation of arthritogenic peptide to antigen-specific T cells by fibroblast-like synoviocytes." Arthritis & Rheumatism 56(5): 1497-1506. <http://hdl.handle.net/2027.42/56038> | en_US |
dc.identifier.issn | 0004-3591 | en_US |
dc.identifier.issn | 1529-0131 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/56038 | |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=17469112&dopt=citation | en_US |
dc.description.abstract | Objective To assess the ability of rheumatoid arthritis (RA) fibroblast-like synoviocytes (FLS) to function as antigen-presenting cells (APCs) for arthritogenic autoantigens found within inflamed joint tissues. Methods Human class II major histocompatibility complex (MHC)–typed FLS were used as APCs for murine class II MHC–restricted CD4 T cell hybridomas. Interferon-Γ (IFNΓ)–treated, antigen-loaded FLS were cocultured with T cell hybridomas specific for immunodominant portions of human cartilage gp-39 (HC gp-39) or human type II collagen (CII). T cell hybridoma activation was measured by enzyme-linked immunosorbent assay of culture supernatants for interleukin-2. Both synthetic peptide and synovial fluid (SF) were used as sources of antigen. APC function in cocultures was inhibited by using blocking antibodies to human class II MHC, CD54, or CD58, or to murine CD4, CD11a, or CD2. Results Human FLS could present peptides from the autoantigens HC gp-39 and human CII to antigen-specific MHC-restricted T cell hybridomas. This response required pretreatment of FLS with IFNΓ, showed MHC restriction, and was dependent on human class II MHC and murine CD4 for effective antigen presentation. Furthermore, FLS were able to extract and present antigens found within human SF to both the HC gp-39 and human CII T cell hybridomas in an IFNΓ-dependent and MHC-restricted manner. Conclusion RA FLS can function as APCs and are able to present peptides derived from autoantigens found within joint tissues to activated T cells in vitro. In the context of inflamed synovial tissues, FLS may be an important and hitherto overlooked subset of APCs that could contribute to autoreactive immune responses. | en_US |
dc.format.extent | 295274 bytes | |
dc.format.extent | 3118 bytes | |
dc.format.mimetype | application/pdf | |
dc.format.mimetype | text/plain | |
dc.publisher | Wiley Subscription Services, Inc., A Wiley Company | en_US |
dc.subject.other | Life and Medical Sciences | en_US |
dc.title | Presentation of arthritogenic peptide to antigen-specific T cells by fibroblast-like synoviocytes | en_US |
dc.type | Article | en_US |
dc.rights.robots | IndexNoFollow | en_US |
dc.subject.hlbsecondlevel | Geriatrics | en_US |
dc.subject.hlbtoplevel | Health Sciences | en_US |
dc.description.peerreviewed | Peer Reviewed | en_US |
dc.contributor.affiliationum | University of Michigan Rheumatic Disease Core Center, Ann Arbor ; University of Michigan Medical School, Ann Arbor | en_US |
dc.contributor.affiliationum | University of Michigan Rheumatic Disease Core Center, Ann Arbor ; University of Michigan Medical School, Ann Arbor | en_US |
dc.contributor.affiliationum | University of Michigan Rheumatic Disease Core Center, Ann Arbor ; University of Michigan Medical School, Ann Arbor | en_US |
dc.contributor.affiliationum | University of Michigan Rheumatic Disease Core Center, Ann Arbor ; University of Michigan Medical School, Ann Arbor | en_US |
dc.contributor.affiliationum | University of Michigan Rheumatic Disease Core Center, Ann Arbor ; University of Michigan Medical School, Ann Arbor | en_US |
dc.contributor.affiliationum | University of Michigan Rheumatic Disease Core Center, Ann Arbor ; University of Michigan Medical School, Ann Arbor | en_US |
dc.contributor.affiliationum | University of Michigan Rheumatic Disease Core Center, Ann Arbor ; University of Michigan Medical School, Ann Arbor | en_US |
dc.contributor.affiliationum | University of Michigan Rheumatic Disease Core Center, Ann Arbor ; University of Michigan Medical School, Ann Arbor | en_US |
dc.contributor.affiliationum | University of Michigan Rheumatic Disease Core Center, Ann Arbor ; University of Michigan Medical School, Ann Arbor | en_US |
dc.contributor.affiliationum | University of Michigan Rheumatic Disease Core Center, Ann Arbor ; University of Michigan Medical School, Ann Arbor | en_US |
dc.contributor.affiliationum | University of Michigan Rheumatic Disease Core Center, Ann Arbor ; University of Michigan Medical School, Ann Arbor ; University of Michigan, Room 3918 Taubman Center, 1500 East Medical Center Drive, Ann Arbor, MI 48109-0358 | en_US |
dc.contributor.affiliationother | Beckman Research Institute, Duarte, California | en_US |
dc.identifier.pmid | 17469112 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/56038/1/22573_ftp.pdf | en_US |
dc.identifier.doi | http://dx.doi.org/10.1002/art.22573 | en_US |
dc.identifier.source | Arthritis & Rheumatism | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
Files in this item
Remediation of Harmful Language
The University of Michigan Library aims to describe library materials in a way that respects the people and communities who create, use, and are represented in our collections. Report harmful or offensive language in catalog records, finding aids, or elsewhere in our collections anonymously through our metadata feedback form. More information at Remediation of Harmful Language.
Accessibility
If you are unable to use this file in its current format, please select the Contact Us link and we can modify it to make it more accessible to you.