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Background  The chemokine receptor CCR5 has been detected at elevated levels on synovial T cells, and a 32 bp deletion in the  CCR5  gene leads to a non-functional receptor. A negative association between the  CCR5Δ32  and rheumatoid arthritis (RA) has been reported, although with conflicting results. In juvenile idiopathic arthritis (JIA), an association with CCR5 was recently reported. The purpose of this study was to investigate if the  CCR5Δ32  polymorphism is associated with RA or JIA in Norwegian cohorts.    Methods  853 RA patients, 524 JIA patients and 658 controls were genotyped for the  CCR5Δ32  polymorphism.    Results  The  CCR5Δ32  allele frequency was 11.5% in the controls vs. 10.4% in RA patients (OR = 0.90;  P  = 0.36) and 9.7% in JIA patients (OR = 0.85;  P  = 0.20). No decreased homozygosity was observed for  CCR5Δ32 , as previously suggested.    Conclusion  Our data do not support an association between the  CCR5Δ32  allele and Norwegian RA or JIA patients. Combining our results with those from a recently published meta-analysis still provide evidence for a role for  CCR5Δ32  in RA, albeit substantially weaker than the effect first reported.

Lack of association between the chemokine receptor 5 polymorphism CCR5delta32 in rheumatoid arthritis and juvenile idiopathic arthritis