Association of rheumatoid arthritis with a functional chemokine receptor, CCR5

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Abstract
Objective To investigate whether the pathogenesis of rheumatoid arthritis (RA) is associated with the functional chemokine receptor CCR5, which is the primary CC chemokine receptor expressed by T cells in rheumatoid synovium, and its nonfunctional receptor, Δ32CCR5, which is generated by the homozygous 32‐basepair deletion (Δ32) in the CCR5 gene. Methods The frequency of the CCR5 genotype was compared among 673 patients with RA, 113 patients with systemic lupus erythematosus (SLE), and 815 control subjects. The CCR5 genotype was studied by polymerase chain reaction amplification of the region flanking the Δ32 deletion (Δ32CCR5). Results Frequencies of the wild‐type CCR5 alleles (0.929, 0.907, and 0.942, respectively) and Δ32CCR5 alleles (0.071, 0.093, and 0.058, respectively) in controls, SLE patients, and RA patients did not differ significantly. However, none of the RA patients had the homozygous Δ32CCR5 genotype, compared with a frequency of 0.009 in controls (P = 0.014 by Fisher's exact test; χ2 = 4.12 with Yates' correction, P = 0.042) and 0.027 in SLE patients (P = 0.003 by Fisher's exact test; χ2= 11.63 with Yates' correction, P = 0.0006). Conclusion The results suggest that the CCR5 receptor plays an important role in RA and may be a suitable target for therapy.