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STAT3 and NF-kappa B signal pathway is required for IL-23-mediated IL-17 production in spontaneous arthritis animal model IL-1 receptor antagonist-deficient mice SCIE SCOPUS

Title
STAT3 and NF-kappa B signal pathway is required for IL-23-mediated IL-17 production in spontaneous arthritis animal model IL-1 receptor antagonist-deficient mice
Authors
Cho, MLKang, JWMoon, YMNam, HJJhun, JYHeo, SBJin, HTMin, SYJu, JHPark, KSCho, YGYoon, CHPark, SHSung, YCKim, HY
Date Issued
2006-05-01
Publisher
AMER ASSOC IMMUNOLOGISTS
Abstract
IL-23 is a heterodimeric cytokine composed of a p19 subunit and the p40 subunit of IL-12. IL-23 has proinflammatory activity, inducing IL-17 secretion from activated CD4(+) T cells and stimulating the proliferation of memory CD4(+) T cells. We investigated the pathogenic role of IL-23 in CD4(+) T cells in mice lacking the IL-1R antagonist (1L-1Ra(-/-)), an animal model of spontaneous arthritis. IL-23 was strongly expressed in the inflamed joints of IL-1Ra(-/-) mice. Recombinant adenovirus expressing mouse IL-23 (rAd/mIL-23) significantly accelerated this joint inflammation and joint destruction. IL-1 beta further increased the production of IL-23, which induced IL-17 production and OX40 expression in splenic CD4(+) T cells of IL-1Ra(-/-) mice. Blocking IL-23 with anti-p19 Ab abolished the IL-17 production induced by IL-1 in splenocyte cultures. The process of IL-23-induced IL-17 production in CD4(+) T cells was mediated via the activation of Jak2, PI3K/Akt, STAT3, and NF-kappa B, whereas p38 MAPK and AP-1 did not participate in the process. Our data suggest that IL-23 is a link between IL-1 and IL-17. IL-23 seems to be a central proinflammatory cytokine in the pathogenesis of this IL-1Ra(-/-) model of spontaneous arthritis. Its intracellular signaling pathway could be useful therapeutic targets in the treatment of autoimmune arthritis.
Keywords
EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; COLONY-STIMULATING FACTOR; CENTRAL-NERVOUS-SYSTEM; T-CELLS; RHEUMATOID-ARTHRITIS; PHOSPHATIDYLINOSITOL 3-KINASE; INFLAMMATORY DEMYELINATION; DESTRUCTIVE ARTHRITIS; SYNOVIAL FIBROBLASTS; CROSS-TALK
URI
https://oasis.postech.ac.kr/handle/2014.oak/23941
DOI
10.4049/jimmunol.176.9.5652
ISSN
0022-1767
Article Type
Article
Citation
JOURNAL OF IMMUNOLOGY, vol. 176, no. 9, page. 5652 - 5661, 2006-05-01
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성영철SUNG, YOUNG CHUL
Dept of Life Sciences
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