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This article is part of the supplement: Proceedings of the 8th Global Arthritis Research Network (GARN) Meeting and 1st Bio-Rheumatology International Congress (BRIC)

Oral presentation

Overview of osteoimmunology: What's happened? And what's going on?

Hiroshi Takayanagi

  • Correspondence: Hiroshi Takayanagi

Author Affiliations

Tokyo Medical and Dental University, ERATO, Japan

Arthritis Research & Therapy 2012, 14(Suppl 1):O12  doi:10.1186/ar3567


The electronic version of this article is the complete one and can be found online at: http://arthritis-research.com/content/14/S1/O12


Published:9 February 2012

© 2012 Takayanagi; licensee BioMed Central Ltd.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Oral presentation

The interaction between the immune and skeletal systems has long been acknowledged, but molecular mechanisms linking the two systems have not been demonstrated until recently. Investigation into autoimmune arthritis as well as the various bone phenotypes found in mice deficient in immunomodulatory molecules has highlighted the importance of the dynamic interplay between the two systems and brought about a rapid evolution of the field of osteoimmunology [1]. In bone loss in autoimmune arthritis, IL-17-producing helper T (TH17) cells play a major role by inducing RANKL [2]. Maintenance and mobilization of hematopoietic cells are regulated by bone cells. In addition to cellular interactions via cytokines, the immune and skeletal systems share various molecules, including transcription factors, signaling molecules and membrane receptors. RANKL stimulates osteoclastogenesis through NFATc1 in cooperation with immunoglobulin-like receptors. Here I will discuss emerging topics in osteoimmunology including the mechanisms underlying bone cell communication: osteocyte RANKL [3] and inhibition of bone formation by osteoclast Sema4D [4].

References

  1. Nat Rev Immunol

    2007, 7:292-304.

  2. Nat Rev Rheumatol

    2009, 5:667-76.

  3. Nat Med

    2011, 17:1231-34.

  4. Nat Med

    2011, 17:1473-80.