Journal
AUTOIMMUNITY REVIEWS
Volume 12, Issue 5, Pages 554-557Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.autrev.2012.10.001
Keywords
CXCL10; Rheumatoid arthritis; Osteoclast; CXCR3; RANKL
Categories
Funding
- MKE/KEIT RD Program [10035615]
- World Class University program of MEST
- NRF [R31-2008-000-10103-0]
Ask authors/readers for more resources
There are several chemokines and their receptors involved in the pathogenesis of chronic inflammatory arthritis. Of those, CXCL10 and its receptor, CXCR3, are increased in many kinds of chronic inflammatory arthritis, especially in rheumatoid arthritis (RA). CXCL10 and CXCR3 play important roles in leukocyte homing to inflamed tissues and in the perpetuation of inflammation, and therefore, tissue damage. In addition to its chemotactic effect, CXCL10 may have pleiotropic functions. Our recent studies show that the crosstalk between CXCL10 and receptor activator of NF-kappa B ligand (RANKL) in inflamed synovial tissue may induce and perpetuate bone destruction in RA. The interaction between CXCL10 and tumor necrosis factor-alpha (TNF-alpha) can also contribute to sustained inflammation in RA. One human trial with anti-CXCL10 monoclonal antibody showed therapeutic potential of blocking CXCL10 in RA treatment. Understanding the novel interaction between this chemokine and other chemokines or cytokines may add possible therapeutic applications in inflammatory arthritis. (C) 2012 Elsevier B.V. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available