Article Text
Abstract
Recent data are presented which indicate a critical role for interleukin (IL)-18 in rheumatoid arthritis (RA). The T cells and macrophages invading the synovium or in the synovial fluid are the chief cellular targets of IL-18 in RA. Neutrophils, dendritic cells and endothelial cells may also be cellular mediators of IL-18. The direct effect of IL-18 on fibroblast-like synoviocytes or chondrocytes may not be essential or important. In RA, IL-18, which is mainly produced by macrophages, activates T cells and macrophages to produce proinflammatory cytokines, chemokines, adhesion molecules and RANKL which, in turn, perpetuate chronic inflammation and induce bone and cartilage destruction.
Statistics from Altmetric.com
Footnotes
Competing interests: None declared.
This study was supported in part by grants from National Natural Science Foundation of China (No. 30672112) and Shanghai Pujiang Talent Program (No. 06PJ14121).
- Abbreviations:
- CIA
- collagen induced arthritis
- DC
- dendritic cell
- GM-CSF
- granulocyte-macrophage colony stimulating factor
- ICAM-1
- intercellular adhesion molecule-1
- IFNγ
- interferon γ
- IL
- interleukin
- IL-18BP
- IL-18 binding protein
- IL-18R
- IL-18 receptor
- MCP-1
- monocyte chemotactic protein-1
- MIP-1α
- macrophage inflammatory protein-1α
- MMP
- metalloproteinase
- NK
- natural killer
- OA
- osteoarthritis
- RA
- rheumatoid arthritis
- RANKL, receptor activator of NFκB ligand; SCW
- streptococcal cell wall
- TLR
- Toll-like receptor
- TNF
- tumour necrosis factor
- VCAM-1
- vascular cell adhesion molecule-1