ヤマナカ　ヒサシ   Yamanaka Hisashi   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