| Osteoclasts in arthritis and Th17 cell development. | |
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MedLine Citation:
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PMID: 21081190 Owner: NLM Status: In-Data-Review |
Abstract/OtherAbstract:
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Bone destruction associated with rheumatoid arthritis (RA) is mainly attributed to the abnormal activation of osteoclasts, which are terminally differentiated cells of monocyte/macrophage lineage that resorb bone matrix. Studies on the immune regulation of osteoclasts in RA have promoted the new research field of "osteoimmunology", which investigates the interplay of the skeletal and immune systems at the molecular level. This interdisciplinary field is proving to be crucial to advances in the treatment of diseases associated with the bone and/or immune systems. As for the mechanisms of the bone destruction found in RA, accumulating evidence lends support to the theory that interleukin (IL)-17-producing helper T (Th17) cells induce the expression of receptor activator of nuclear factor-κB ligand (RANKL) in synovial cells, which in turn stimulates the differentiation and activation of osteoclasts together with inflammatory cytokines. Thus, inhibition of Th17 is potentially beneficial for the amelioration of the bone damage which occurs in RA. A recent study revealed that IκBζ is essential to the development of Th17 cells. These findings comprise an important advance in our understanding of the pathogenesis of RA and potentially effective therapeutic strategies. |
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Authors:
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Kazuo Okamoto; Hiroshi Takayanagi |
Publication Detail:
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Type: Journal Article Date: 2010-11-26 |
Journal Detail:
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Title: International immunopharmacology Volume: 11 ISSN: 1878-1705 ISO Abbreviation: Int. Immunopharmacol. Publication Date: 2011 May |
Date Detail:
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Created Date: 2011-04-18 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 100965259 Medline TA: Int Immunopharmacol Country: Netherlands |
Other Details:
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Languages: eng Pagination: 543-8 Citation Subset: IM |
Copyright Information:
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Copyright © 2010 Elsevier B.V. All rights reserved. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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