REVIEW

Cellular targets of interleukin-18 in rheumatoid arthritis

Sheng-Ming Dai¹, Zheng-Zheng Shan¹, Huji Xu², Kusuki Nishioka³

¹ Department of Rheumatology and Immunology, Changhai Hospital, Second Military Medical University, Shanghai, China
² Department of Rheumatology and Immunology, Changzheng Hospital, Second Military Medical University, Shanghai, China
³ Department of Bioregulation, Institute of Medical Science, St Marianna University School of Medicine, Kawasaki, Japan

Dr Sheng-Ming Dai, Department of Rheumatology and Immunology, Changhai Hospital, Second Military Medical University, 174 Changhai Road, Shanghai 200433, P R China; dsm{at}medmail.com.cn

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.

Abbreviations: CIA, collagen induced arthritis; DC, dendritic cell; GM-CSF, granulocyte-macrophage colony stimulating factor; ICAM-1, intercellular adhesion molecule-1; IFN, interferon ; IL, interleukin; IL-18BP, IL-18 binding protein; IL-18R, IL-18 receptor; MCP-1, monocyte chemotactic protein-1; MIP-1, macrophage inflammatory protein-1; MMP, metalloproteinase; NK, natural killer; OA, osteoarthritis; RA, rheumatoid arthritis; RANKL, receptor activator of NFB ligand; SCW, streptococcal cell wall; TLR, Toll-like receptor; TNF, tumour necrosis factor; VCAM-1, vascular cell adhesion molecule-1

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