The Journal of Experimental Medicine
StemCell Technologies
  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents
Published online 6 November 2006 doi:10.1084/jem.20061775
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 203, Number 12, 2673-2682
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Supplemental Material Index
Right arrow Alert me when this article is cited
Right arrow Citation Map
Services
Right arrow Email this article
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new content in the JEM
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Sato, K.
Right arrow Articles by Takayanagi, H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Sato, K.
Right arrow Articles by Takayanagi, H.
Related Collections
Right arrowRelated Article
Social Bookmarking
Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?

ARTICLE

 Th17 functions as an osteoclastogenic helper T cell subset that links T cell activation and bone destruction

Kojiro Sato1,3, Ayako Suematsu1,3, Kazuo Okamoto1,3, Akira Yamaguchi2, Yasuyuki Morishita4, Yuho Kadono5, Sakae Tanaka5, Tatsuhiko Kodama6, Shizuo Akira7, Yoichiro Iwakura8, Daniel J. Cua9, and Hiroshi Takayanagi1,3,10

1 Department of Cell Signaling, 2 Department of Oral Pathology, Graduate School, and 3 COE Program for Frontier Research on Molecular Destruction and Reconstruction of Tooth and Bone, Tokyo Medical and Dental University, Tokyo 113-8549, Japan
4 Department of Human Pathology and 5 Department of Orthopaedic Surgery, Graduate School of Medicine, University of Tokyo, Tokyo 113-0033, Japan
6 Department of Systems Biology and Medicine, Research Center for Advanced Science and Technology, University of Tokyo, Tokyo 153-8904, Japan
7 Department of Host Defence, Research Institute for Microbial Diseases, Osaka University, Osaka 565-0871, Japan
8 Center for Experimental Medicine, Institute of Medical Science, University of Tokyo, Tokyo 108-8639, Japan
9 Discovery Research, DNAX Research Inc., Palo Alto, CA 94304
10 Solution Oriented Research for Science and Technology (SORST), Japan Science and Technology Agency (JST), Saitama 332-0012, Japan

CORRESPONDENCE Hiroshi Takayanagi: taka.csi{at}tmd.ac.jp

In autoimmune arthritis, traditionally classified as a T helper (Th) type 1 disease, the activation of T cells results in bone destruction mediated by osteoclasts, but how T cells enhance osteoclastogenesis despite the anti-osteoclastogenic effect of interferon (IFN)-{gamma} remains to be elucidated. Here, we examine the effect of various Th cell subsets on osteoclastogenesis and identify Th17, a specialized inflammatory subset, as an osteoclastogenic Th cell subset that links T cell activation and bone resorption. The interleukin (IL)-23–IL-17 axis, rather than the IL-12–IFN-{gamma} axis, is critical not only for the onset phase, but also for the bone destruction phase of autoimmune arthritis. Thus, Th17 is a powerful therapeutic target for the bone destruction associated with T cell activation.

Abbreviations used: BMC, BM cell; BMM, BM-derived monocyte/macrophage precursor cell; M-CSF, macrophage colony-stimulating factor; MNC; multinucleated cell; PGE2, prostaglandin E2; RA, rheumatoid arthritis; RANKL, receptor activator of NF-{kappa}B ligand; TRAP, tartrate-resistant acid phosphatase; T reg, regulatory T; VitD3, 1,25 (OH)2 vitamin D3.


Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?

Related Article

Bone destruction by Th17
Ruth Williams
J. Exp. Med. 2006 203: 2567. [Full Text] [PDF]



This article has been cited by other articles:



  Home | Help | Feedback | Subscriptions | Archive | Search
TABLE OF CONTENTS