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Regulation of bone by the adaptive immune system in arthritis

Kazuo Okamoto123 and Hiroshi Takayanagi1234*

Author Affiliations

1 Department of Cell Signaling, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Yushima 1-5-45, Bunkyo-ku, Tokyo 113-8549, Japan

2 Global Center of Excellence (GCOE) Program, International Research Center for Molecular Science in Tooth and Bone Diseases, Yushima 1-5-45, Bunkyo-ku, Tokyo 113-8549, Japan

3 Japan Science and Technology Agency (JST), ERATO, Takayanagi Osteonetwork Project, Yushima 1-5-45, Bunkyo-ku, Tokyo 113-8549, Japan

4 Centre for Orthopaedic Research, School of Surgery, The University of Western Australia, Monash Ave, Nedlands, WA 6009, Australia

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Arthritis Research & Therapy 2011, 13:219  doi:10.1186/ar3323

Published: 27 May 2011


Studies on the immune regulation of osteoclasts in rheumatoid arthritis have promoted the new research field of 'osteoimmunology', which investigates the interplay between the skeletal and immune systems at the molecular level. Accumulating evidence lends support to the theory that bone destruction associated with rheumatoid arthritis is caused by the enhanced activity of osteoclasts, resulting from the activation of a unique helper T cell subset, 'Th17 cells'. Understanding the interaction between osteoclasts and the adaptive immune system in rheumatoid arthritis and the molecular mechanisms of Th17 development will lead to the development of potentially effective therapeutic strategies.