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Arthritis
Volume 2012 (2012), Article ID 713618, 6 pages
doi:10.1155/2012/713618
Pathological Role of Interleukin-6 in Psoriatic Arthritis
1Department of Respiratory Medicine, Allergy and Rheumatic Diseases, Osaka University Graduate School of Medicine, Osaka 565-0871, Japan
2Department of Immunopathology, WPI Immunology Frontier Research Center, Osaka University, Osaka 565-0871, Japan
3Department of Clinical Application of Biologics, Osaka University Graduate School of Medicine, Osaka 565-0871, Japan
Received 29 August 2012; Accepted 4 October 2012
Academic Editor: Ruben Burgos-Vargas
Copyright © 2012 Atsushi Ogata et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
Psoriatic arthritis (PsA) is a clinical manifestation of psoriatic disease. Although the pathogenesis of PsA remains unknown, PsA can be managed by treatments similar to those used for rheumatoid arthritis (RA). Because interleukin-(IL-) 6 has been suggested to have a pathogenic role in PsA, a humanized anti-IL-6 receptor antibody tocilizumab treatment for PsA was recently tried. However, the efficacy of tocilizumab for PsA was not favorable. This suggests that the pathogenic roles of IL-6 in PsA and RA are different. In RA, tumor necrosis factor (TNF) primarily contributes to the arthritis effector phase and IL-6 contributes to the arthritis priming phase. In PsA, the TNF-related effector phase is similar to that in RA, but the IL-6-related priming phase might not be critical. This paper discusses the role of IL-6 in PsA.