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J. Clin. Med. 2017, 6(9), 81; doi:10.3390/jcm6090081

IL-23 and Th17 Disease in Inflammatory Arthritis

Institute of Rheumatology, Tokyo Women’s Medical University 10-22 Kawada-cho, Shinjuku-ku, Tokyo 162-0054, Japan
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Academic Editor: Emmanuel Andrès
Received: 29 April 2017 / Revised: 6 July 2017 / Accepted: 26 August 2017 / Published: 29 August 2017
(This article belongs to the Special Issue Th17 Cell in Autoimmune and Inflammatory Diseases)
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Abstract

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. View Full-Text
Keywords: IL-23; rheumatoid arthritis; spondyloarthritis; ankylosing spondylitis; psoriatic arthritis IL-23; rheumatoid arthritis; spondyloarthritis; ankylosing spondylitis; psoriatic arthritis
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MDPI and ACS Style

Yago, T.; Nanke, Y.; Kawamoto, M.; Kobashigawa, T.; Yamanaka, H.; Kotake, S. IL-23 and Th17 Disease in Inflammatory Arthritis. J. Clin. Med. 2017, 6, 81.

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