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.
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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).
- collagen induced arthritis
- dendritic cell
- granulocyte-macrophage colony stimulating factor
- intercellular adhesion molecule-1
- interferon γ
- IL-18 binding protein
- IL-18 receptor
- monocyte chemotactic protein-1
- macrophage inflammatory protein-1α
- natural killer
- rheumatoid arthritis
- RANKL, receptor activator of NFκB ligand; SCW
- streptococcal cell wall
- Toll-like receptor
- tumour necrosis factor
- vascular cell adhesion molecule-1
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