Journal
GENES AND IMMUNITY
Volume 7, Issue 3, Pages 264-268Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/sj.gene.6364298
Keywords
rheumatoid arthritis; CCR5; association; case-control; meta-analysis; chemokines
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Funding
- NCRR NIH HHS [M01 RR000064-410677, M01-RR00064, M01 RR000064] Funding Source: Medline
- NIAMS NIH HHS [K23 AR50177, K23 AR050177, K23 AR050177-02] Funding Source: Medline
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Rheumatoid arthritis (RA) is characterized by synovial inflammation mediated by T-cells, monocytes and macrophages. The homing of these cells to the inflamed synovium is regulated by chemokine-receptors and their ligands. A 32-basepair deletion (Delta 32) in the gene encoding CCR5, a chemokine-receptor, results in a non-functional receptor. A negative association between CCR5-Delta 32 and RA has been described, although other studies found no associations. Furthermore, the observation that individuals homozygous for CCR5-Delta 32 develop RA has raised questions about the role of CCR5-Delta 32. This meta-analysis of all published case-control association studies confirms the negative association between CCR5-Delta 32 and RA (Odds Ratio = 0.65; 95% confidence intervals = 0.55-0.77; P < 0.0001), suggesting that CCR5-Delta 32 is protective against the development of RA. CCR5 blockade in animal models of RA results in amelioration of arthritis, suggesting that CCR5 blockade could also modify disease in patients with RA.
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