ヤマナカ ヒサシ
  山中 寿
   所属   医学部 医学科(東京女子医科大学病院)
   職種   客員教授
論文種別 総説
言語種別 英語
査読の有無 査読あり
表題 IL-23 and Th17 Disease in Inflammatory Arthritis.
掲載誌名 正式名:Journal of clinical medicine
略  称:J Clin Med
ISSNコード:(2077-0383)2077-0383(Linking)
掲載区分国外
巻・号・頁 6(9),pp.piiE81
著者・共著者 Yago Toru, Nanke Yuki, Kawamoto Manabu, Kobashigawa Tsuyoshi, Yamanaka Hisashi, Kotake Shigeru
発行年月 2017/08
概要 IL-23, which is composed of p19 and p40 subunits, is a proinflammatory cytokine that contributes to the formation and maintenance of Th17 cells in inflammatory autoimmune diseases. IL-23 is a human osteoclastogenic cytokine and anti-IL-23 antibody attenuates paw volume and joint destruction in CIA rats. IL-23 levels in serum and synovial fluid are high in rheumatoid arthritis (RA) patients, and IL-23 may be a useful biomarker for the diagnosis of RA. In addition, IL-23 affects the pathogenesis of inflammation and bone destruction through interaction with other cytokines such as IL-17 and TNF-α. Furthermore, polymorphisms of IL23R are a risk factor for ankylosing spondylitis (AS) and psoriatic arthritis (PsA), which indicates that IL-23 is also involved in the pathogenesis of spondyloarthritis (SpA). Finally, IL-17 and IL-23 inhibitors reduce the clinical manifestations of SpA. Thus, the IL-23/Th17 pathway is a therapeutic target for the treatment of inflammatory arthritis.
DOI 10.3390/jcm6090081
PMID 28850053