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Osteoclasts in arthritis and Th17 cell development.

Abstract：

: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.

journal_name

Int Immunopharmacol

journal_title

International immunopharmacology

authors

Okamoto K,Takayanagi H

doi

10.1016/j.intimp.2010.11.010

subject

Has Abstract

pub_date

2011-05-01 00:00:00

pages

543-8

issue

5

eissn

1567-5769

issn

1878-1705

pii

S1567-5769(10)00358-9

journal_volume

11

pub_type

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