Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 윤지희 | - |
dc.date.accessioned | 2018-04-19T08:42:55Z | - |
dc.date.available | 2018-04-19T08:42:55Z | - |
dc.date.issued | 2012-03 | - |
dc.identifier.citation | Arthritis & Rheumatism, 2012, 64(3), P.740-751 | en_US |
dc.identifier.issn | 2326-5205 | - |
dc.identifier.uri | https://onlinelibrary.wiley.com/doi/abs/10.1002/art.33390 | - |
dc.identifier.uri | https://repository.hanyang.ac.kr/handle/20.500.11754/69552 | - |
dc.description.abstract | Objective Bone destruction is a critical pathology involved in the functional disability caused by rheumatoid arthritis (RA). Osteoclasts, which are specialized bone-resorbing cells regulated by cytokines such as RANKL, are implicated in bone destruction in RA. The aim of this study was to determine whether interleukin-21 (IL-21), a potent immunomodulatory 4a-helical bundle type 1 cytokine, has osteoclastogenic activity in patients with RA and in mice with collagen-induced arthritis (CIA). Methods. The expression of IL-21 in synovial tissue was examined using immunohistochemistry. The concentrations of IL-21 in serum and synovial fluid were determined by enzyme-linked immunosorbent assay. The levels of RANKL and osteoclastogenic markers were measured using real-time polymerase chain reaction. CD14+ monocytes from patients with RA or mouse bone marrow cells were cocultured with fibroblast-like synoviocytes (FLS) from patients with RA or CD4+ T cells from mice with CIA in the presence of IL-21 and subsequently stained for tartrate-resistant acid phosphatase activity to determine osteoclast formation. Results. IL-21 was up-regulated in the synovium, synovial fluid, and serum of patients with RA and in the synovium and serum of mice with CIA. IL-21 induced RANKL expression in mixed joint cells and CD4+ T cells from mice with CIA and in CD4+ T cells and FLS from patients with RA. Moreover, IL-21 enhanced in vitro osteoclastogenesis without the presence of RANKL-providing cells and by inducing RANKL expression in CD4+ T cells and FLS. Conclusion. Our data suggest that IL-21 promotes osteoclastogenesis in RA. We believe that therapeutic strategies targeting IL-21 might be effective for the treatment of patients with RA, especially in preventing bone destruction. | en_US |
dc.language.iso | en | en_US |
dc.publisher | Wiley-Blackwell | en_US |
dc.subject | SYSTEMIC-LUPUS-ERYTHEMATOSUS | en_US |
dc.subject | NECROSIS-FACTOR-ALPHA | en_US |
dc.subject | T-CELL-ACTIVATION | en_US |
dc.subject | BXSB-YAA MICE | en_US |
dc.subject | RECEPTOR ACTIVATOR | en_US |
dc.subject | BONE DESTRUCTION | en_US |
dc.subject | SYNOVIAL FIBROBLASTS | en_US |
dc.subject | RADIOLOGIC DAMAGE | en_US |
dc.subject | TH17 CELLS | en_US |
dc.subject | IL-21 | en_US |
dc.title | Interleukin-21 promotes osteoclastogenesis in humans with rheumatoid arthritis and in mice with collagen-induced arthritis | en_US |
dc.type | Article | en_US |
dc.relation.no | 3 | - |
dc.relation.volume | 64 | - |
dc.identifier.doi | 10.1002/art.33390 | - |
dc.relation.page | 740-751 | - |
dc.relation.journal | ARTHRITIS AND RHEUMATISM | - |
dc.contributor.googleauthor | Kwok, S. K. | - |
dc.contributor.googleauthor | Cho, M. L. | - |
dc.contributor.googleauthor | Park, M. K. | - |
dc.contributor.googleauthor | Oh, H. J. | - |
dc.contributor.googleauthor | Park, J. S. | - |
dc.contributor.googleauthor | Her, Y. M. | - |
dc.contributor.googleauthor | Lee, S. Y. | - |
dc.contributor.googleauthor | Youn, J. | - |
dc.contributor.googleauthor | Ju, J. H. | - |
dc.contributor.googleauthor | Park, K. S. | - |
dc.relation.code | 2012201020 | - |
dc.sector.campus | S | - |
dc.sector.daehak | COLLEGE OF MEDICINE[S] | - |
dc.sector.department | DEPARTMENT OF MEDICINE | - |
dc.identifier.pid | jhyoun | - |
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