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10.3390/jcm6090081

http://scihub22266oqcxt.onion/10.3390/jcm6090081
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C5615274!5615274!28850053
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suck abstract from ncbi

pmid28850053      J+Clin+Med 2017 ; 6 (9): ä
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  • IL-23 and Th17 Disease in Inflammatory Arthritis #MMPMID28850053
  • Yago T; Nanke Y; Kawamoto M; Kobashigawa T; Yamanaka H; Kotake S
  • J Clin Med 2017[Sep]; 6 (9): ä PMID28850053show ga
  • 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-?. 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.
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