IL-23 and Th17 Disease in Inflammatory Arthritis
AbstractIL-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
Share & Cite This Article
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.
Yago T, Nanke Y, Kawamoto M, Kobashigawa T, Yamanaka H, Kotake S. IL-23 and Th17 Disease in Inflammatory Arthritis. Journal of Clinical Medicine. 2017; 6(9):81.Chicago/Turabian Style
Yago, Toru; Nanke, Yuki; Kawamoto, Manabu; Kobashigawa, Tsuyoshi; Yamanaka, Hisashi; Kotake, Shigeru. 2017. "IL-23 and Th17 Disease in Inflammatory Arthritis." J. Clin. Med. 6, no. 9: 81.
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.