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IL-23 and Th17 Disease in Inflammatory Arthritis

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 r...

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Autores principales: Yago, Toru, Nanke, Yuki, Kawamoto, Manabu, Kobashigawa, Tsuyoshi, Yamanaka, Hisashi, Kotake, Shigeru
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5615274/
https://www.ncbi.nlm.nih.gov/pubmed/28850053
http://dx.doi.org/10.3390/jcm6090081
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author Yago, Toru
Nanke, Yuki
Kawamoto, Manabu
Kobashigawa, Tsuyoshi
Yamanaka, Hisashi
Kotake, Shigeru
author_facet Yago, Toru
Nanke, Yuki
Kawamoto, Manabu
Kobashigawa, Tsuyoshi
Yamanaka, Hisashi
Kotake, Shigeru
author_sort Yago, Toru
collection PubMed
description 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.
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spelling pubmed-56152742017-09-28 IL-23 and Th17 Disease in Inflammatory Arthritis Yago, Toru Nanke, Yuki Kawamoto, Manabu Kobashigawa, Tsuyoshi Yamanaka, Hisashi Kotake, Shigeru J Clin Med Review 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. MDPI 2017-08-29 /pmc/articles/PMC5615274/ /pubmed/28850053 http://dx.doi.org/10.3390/jcm6090081 Text en © 2017 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Yago, Toru
Nanke, Yuki
Kawamoto, Manabu
Kobashigawa, Tsuyoshi
Yamanaka, Hisashi
Kotake, Shigeru
IL-23 and Th17 Disease in Inflammatory Arthritis
title IL-23 and Th17 Disease in Inflammatory Arthritis
title_full IL-23 and Th17 Disease in Inflammatory Arthritis
title_fullStr IL-23 and Th17 Disease in Inflammatory Arthritis
title_full_unstemmed IL-23 and Th17 Disease in Inflammatory Arthritis
title_short IL-23 and Th17 Disease in Inflammatory Arthritis
title_sort il-23 and th17 disease in inflammatory arthritis
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5615274/
https://www.ncbi.nlm.nih.gov/pubmed/28850053
http://dx.doi.org/10.3390/jcm6090081
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