IL-23 P19 Expression Induced by IL-17 and IL-1beta in Rheumatoid Arthritis Synovial Mononuclear Cells
Immune Network
; : 29-37, 2008.
Article
在 Ko
| WPRIM
| ID: wpr-142415
Responsible library:
WPRO
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.
Key words
全文:
1
索引:
WPRIM
主要主题:
Osteoarthritis
/
Arthritis, Rheumatoid
/
Synovial Fluid
/
Synovial Membrane
/
RNA, Messenger
/
Enzyme-Linked Immunosorbent Assay
/
Immunohistochemistry
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RNA-Directed DNA Polymerase
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Tumor Necrosis Factor-alpha
/
Interleukin-17
限制:
Humans
语言:
Ko
期刊:
Immune Network
年:
2008
类型:
Article