Common autoantibody among Takayasu arteritis and ulcerative colitis : a possible pathophysiology that includes gut-vessel connection in vascular inflammation
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DOI[10.31662/jmaj.2023-0038]のデータに遷移します
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- 資料種別
- 記事
- 著者・編者
- Tsuyoshi Shirai
- 出版年月日等
- 2023-07-14
- 出版年（W3CDTF）
- 2023-07-14
- タイトル（掲載誌）
- JMA Journal
- 巻号年月日等（掲載誌）
- 6(3)
- 掲載巻
- 6(3)
- ISSN（掲載誌）
- 2433-3298
- ISSN-L（掲載誌）
- 2433-328X
- 本文の言語コード
- eng
- DOI
- 10.31662/jmaj.2023-0038
- 国立国会図書館永続的識別子
- info:ndljp/pid/14495017
- コレクション（共通）
- コレクション（障害者向け資料：レベル1）
- コレクション（個別）
- 国立国会図書館デジタルコレクション > 電子書籍・電子雑誌 > その他
- 収集根拠
- インターネット資料収集保存事業（WARP）
- 受理日（W3CDTF）
- 2025-10-21T09:04:40+09:00
- 保存日（W3CDTF）
- 2024-09-26
- 記録形式（IMT）
- application/pdf
- オンライン閲覧公開範囲
- インターネット公開
- 遠隔複写可否（NDL）
- 不可
- 掲載誌（国立国会図書館永続的識別子）
- info:ndljp/pid/14495014
- 連携機関・データベース
- 国立国会図書館 : 国立国会図書館デジタルコレクション
- 要約等
- <p>Takayasu arteritis (TAK) is a type of large-vessel vasculitis that predominantly affects young females. The precise pathomechanism of TAK is still under investigation. In TAK, the vasa vasorum is considered to be the initial inflammatory site. Disruption of the vasa vasorum induces the entry of inflammatory cells into the vascular wall of large vessels between the media and adventitia, and infiltrated cells damage the vascular components, eventually leading to stenosis or dilatation of the affected arteries. In addition, T cells are considered key players in TAK, and myeloid cells function as effector cells. Although the roles of B cells in TAK are poorly understood, recent evidence supports their contribution to the pathogenicity of TAK. Particularly, two autoantibodies have been identified in TAK through investigation of anti-endothelial cell antibodies, and they could be involved in the maintenance of vascular inflammation. Furthermore, one of the autoantibodies, anti-endothelial protein C receptor, was shown to be present in ulcerative colitis (UC), which is genetically and clinically associated with TAK. Similar autoantibodies in inflammatory diseases with different target organs indicate a common underlying pathophysiology of these diseases, which could be characterized by the aberrant activation of B cells. This review discusses recent understanding of the pathomechanisms of TAK and UC, with a focus on the involvement of B cells and autoantibodies. The close association of UC with TAK further suggests a common etiology, and the importance of the intestinal microbiota, including dysbiosis, is also becoming known in TAK. Investigation of such common factors among TAK and UC would improve understanding of the interplay between gut and vascular inflammation, which is a new concept for developing vascular inflammation through the gut-vessel connection.</p>
- DOI
- 10.31662/jmaj.2023-0038
- オンライン閲覧公開範囲
- インターネット公開
- 連携機関・データベース
- 科学技術振興機構 : J-STAGE
- 要約等
- <p>Takayasu arteritis (TAK) is a type of large-vessel vasculitis that predominantly affects young females. The precise pathomechanism of TAK is still under investigation. In TAK, the vasa vasorum is considered to be the initial inflammatory site. Disruption of the vasa vasorum induces the entry of inflammatory cells into the vascular wall of large vessels between the media and adventitia, and infiltrated cells damage the vascular components, eventually leading to stenosis or dilatation of the affected arteries. In addition, T cells are considered key players in TAK, and myeloid cells function as effector cells. Although the roles of B cells in TAK are poorly understood, recent evidence supports their contribution to the pathogenicity of TAK. Particularly, two autoantibodies have been identified in TAK through investigation of anti-endothelial cell antibodies, and they could be involved in the maintenance of vascular inflammation. Furthermore, one of the autoantibodies, anti-endothelial protein C receptor, was shown to be present in ulcerative colitis (UC), which is genetically and clinically associated with TAK. Similar autoantibodies in inflammatory diseases with different target organs indicate a common underlying pathophysiology of these diseases, which could be characterized by the aberrant activation of B cells. This review discusses recent understanding of the pathomechanisms of TAK and UC, with a focus on the involvement of B cells and autoantibodies. The close association of UC with TAK further suggests a common etiology, and the importance of the intestinal microbiota, including dysbiosis, is also becoming known in TAK. Investigation of such common factors among TAK and UC would improve understanding of the interplay between gut and vascular inflammation, which is a new concept for developing vascular inflammation through the gut-vessel connection.</p>
- DOI
- 10.31662/jmaj.2023-0038
- オンライン閲覧公開範囲
- インターネット公開
- 関連情報（URI）
- 参照
- Active withdrawal of corticosteroids using tocilizumab and its association with autoantibody profiles in relapsed Takayasu arteritis: a multicentre, single-arm, prospective study (the Ab-TAK study)Anti-integrin αvβ6 antibody in Takayasu arteritis patients with or without ulcerative colitisSystematic Review and Meta-Analysis for JCS 2026 Guideline on Management of Large-Vessel VasculitisAutoantibodies and B Cells in Takayasu Arteritis and Giant Cell Arteritis: Comparative Insights into Large-Vessel Vasculitis
- 連携機関・データベース
- 国立情報学研究所 : CiNii Research
- 提供元機関・データベース
- Japan Link Center雑誌記事索引データベースCrossref科学研究費助成事業データベースCrossrefCrossrefCrossrefCrossref
- 書誌ID（NDLBibID）
- 14495017