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IL-23 P19 Expression Induced by IL-17 and $IL-1{\beta}$ in Rheumatoid Arthritis Synovial Mononuclear Cells  

Cho, Mi-La (Rheumatism Research Center (RhRC), Catholic University)
Heo, Yu-Jung (Rheumatism Research Center (RhRC), Catholic University)
Oh, Hye-Jwa (Rheumatism Research Center (RhRC), Catholic University)
Kang, Chang-Min (Rheumatism Research Center (RhRC), Catholic University)
Lee, Seon-Yeong (Rheumatism Research Center (RhRC), Catholic University)
Hong, Yeon-Sik (Departmrnt of Internal Medicine, Our Lady of Mercy Hospital, Catholic University College of Medicine)
Kim, Ho-Youn (Rheumatism Research Center (RhRC), Catholic University)
Publication Information
IMMUNE NETWORK / v.8, no.1, 2008 , pp. 29-37 More about this Journal
Abstract
Interleukin-23 (IL-23) is a novel pro-inflammatory cytokine which has been implicated to play a pathogenic role in rheumatoid arthritis (RA). This study was undertaken to investigate the IL-23 inductive activity of the proinflammatory cytokine IL-17, $IL-1{\beta}$ and tumor necrosis factor (TNF-${\alpha}$) in RA synovial fluid mononuclear cells (SFMC). Expression of IL-23p19, IL-17, $IL-1{\beta}$ and TNF-${\alpha}$ in joint was examined by immunohistochemistry (IHC) of patients with RA and osteoarthritis (OA). The effects of IL-17 and $IL-1{\beta}$ on expression of IL-23p19 in human SFMC from RA patients were determined by reverse transcriptase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA). IL-23p19 was expressed in the RA fibroblast like synoviocyte (FLS), but not from OA FLS. Similar to the protein expression, IL-23p19 mRNA could be detected by RT-PCR in RA SFMC. IL-17 and $IL-1{\beta}$ could induce RA SFMC to produce the IL-23p19. The effects of IL-17 were much stronger than $IL-1{\beta}$ or TNF-${\alpha}$. These responses were observed in a doseresponsive manner. In addition, IL-17 or $IL-1{\beta}$ neutralizing antibody down-regulated the expression of IL-23p19 induced by LPS in RA-SFMC. Our results demonstrate that IL-23p19 is overexpressed in RA synovium and IL-17 and $IL-1{\beta}$ appears to upregulate the expression of IL-23p19 in RA-SFMC.
Keywords
Rheumatoid arthritis; Synovial fluid mononuclear cells; IL-23p19; IL-17; $IL-1{\beta}$;
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