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タイトル: | A distinct human CD4+ T cell subset that secretes CXCL13 in rheumatoid synovitis. |
著者: | Kobayashi, Shio Murata, Koichi Shibuya, Hideyuki Morita, Mami Ishikawa, Masahiro Furu, Moritoshi Ito, Hiromu Ito, Juichi Matsuda, Shuichi Watanabe, Takeshi Yoshitomi, Hiroyuki https://orcid.org/0000-0001-7339-9030 (unconfirmed) |
著者名の別形: | 吉富, 啓之 |
発行日: | 10-Sep-2013 |
出版者: | John Wiley & Sons, Inc. |
誌名: | Arthritis and rheumatism |
巻: | 65 |
号: | 12 |
開始ページ: | 3063 |
終了ページ: | 3072 |
抄録: | [Objective] ]Human CD4+ T cells in synovitis of rheumatoid arthritis (RA) produce CXCL13, a chemokine crucial for the formation of germinal center. This study was undertaken to determine the relevance of this population to known subsets of helper T cells and to proinflammatory cytokines and how these cells are generated. [Methods] The expression of Th markers and CXCL13 in CD4+ T cells of RA synovitis and the involvement of proinflammatory cytokines in CXCL13 production were assessed. We also investigated whether CXCL13+CD4+ T cells could be newly induced. [Results] CXCL13+CD4+ T cells of RA synovitis were negative for interferon-γ (IFN-γ), interleukin-4 (IL-4), IL-17, Foxp3, and CXCR5, and expressed low levels of ICOS, indicating that this population is a distinct human CD4 subset. T cell receptor (TCR) stimulation of CD4+ T cells from RA synovitis with low expression of CXCL13, promptly induced CXCL13 production, and addition of proinflammatory cytokines supported the long-term production of CXCL13, indicating that CXCL13-producing CD4+ T cells can be in a memory state ready to be reactivated upon TCR stimulation, and that proinflammatory cytokines are involved in persistent CXCL13 production. TCR stimulation of blood CD4+ T cells from healthy volunteers together with proinflammatory cytokines induced a population that produced CXCL13 but not IFN-γ. Synovial T cells recruited CXCR5+ cells in a CXCL13-dependent manner. [Conclusion] CXCL13-producing CD4+ T cells induced in RA synovitis may play a role in the recruitment of CXCR5+ cells, such as B cells and circulating Tfh cells, and in ectopic lymphoid neogenesis in inflammatory sites. |
記述: | 関節リウマチから新たなヘルパーT細胞を同定 -慢性炎症のメカニズム解明に期待-. 京都大学プレスリリース. 2013-09-20. |
著作権等: | © 2013 American College of Rheumatology この論文は出版社版でありません。引用の際には出版社版をご確認ご利用ください。 This is not the published version. Please cite only the published version. |
URI: | http://hdl.handle.net/2433/178763 |
DOI(出版社版): | 10.1002/art.38173 |
PubMed ID: | 24022618 |
関連リンク: | https://www.kyoto-u.ac.jp/static/ja/news_data/h/h1/news6/2013/130920_2.htm |
出現コレクション: | 学術雑誌掲載論文等 |
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