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

류마티스관절염 환자의 활액 세포에서 IL-17과 $IL-1{\beta}$에 의한 IL-23p19의 발현 증가

  • 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)
  • 조미라 (가톨릭대학교 의과대학 류마티스 연구센터) ;
  • 허유정 (가톨릭대학교 의과대학 류마티스 연구센터) ;
  • 오혜좌 (가톨릭대학교 의과대학 류마티스 연구센터) ;
  • 강창민 (가톨릭대학교 의과대학 류마티스 연구센터) ;
  • 이선영 (가톨릭대학교 의과대학 류마티스 연구센터) ;
  • 홍연식 (가톨릭대학교 의과대학 성모자애병원 류마티스내과) ;
  • 김호연 (가톨릭대학교 의과대학 류마티스 연구센터)
  • Published : 2008.03.30

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

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