IL-23 P19 Expression Induced by IL-17 and IL-1beta in Rheumatoid Arthritis Synovial Mononuclear Cells.
- Author:
Mi La CHO
1
;
Yu Jung HEO
;
Hye Jwa OH
;
Chang Min KANG
;
Seon Yeong LEE
;
Yeon Sik HONG
;
Ho Youn KIM
Author Information
- Publication Type:Original Article
- Keywords: Rheumatoid arthritis; Synovial fluid mononuclear cells; IL-23p19; IL-17; IL-1 beta
- MeSH: Antibodies, Neutralizing; Arthritis, Rheumatoid; Enzyme-Linked Immunosorbent Assay; Fibroblasts; Humans; Immunohistochemistry; Interleukin-17; Interleukin-1beta; Interleukin-23; Interleukin-23 Subunit p19; Joints; Osteoarthritis; RNA, Messenger; RNA-Directed DNA Polymerase; Synovial Fluid; Synovial Membrane; Tumor Necrosis Factor-alpha
- From:Immune Network 2008;8(1):29-37
- CountryRepublic of Korea
- Language:Korean
- 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 dose- responsive 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.
