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Nanke Yuki
Department School of Nursing, School of Nursing Position Professor |
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| Article types | Review article |
| Language | English |
| Peer review | Peer reviewed |
| Title | IL-23 and Th17 Disease in Inflammatory Arthritis. |
| Journal | Formal name：Journal of clinical medicine Abbreviation：J Clin Med ISSN code：(2077-0383)2077-0383(Linking) |
| Domestic / Foregin | Foregin |
| Volume, Issue, Page | 6(9),pp.piiE81 |
| Author and coauthor | Yago Toru, Nanke Yuki, Kawamoto Manabu, Kobashigawa Tsuyoshi, Yamanaka Hisashi, Kotake Shigeru |
| Publication date | 2017/08 |
| Summary | 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 |