Research article

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

Ewald Lindner^1* , Gry BN Nordang^1* , Espen Melum¹ , Berit Flatø² , Anne Marit Selvaag² , Erik Thorsby¹ , Tore K Kvien³ , Øystein T Førre² and Benedicte A Lie¹

¹  Institute of Immunology, Rikshospitalet-Radiumhospitalet Medical Center, 0027 Oslo, Norway

²  Department of Rheumatology, Rikshospitalet-Radiumhospitalet Medical Center, 0027 Oslo, Norway

³  Department of Rheumatology, Diakonhjemmet Hospital, N-0319 Oslo, Norway

author email corresponding author email* Contributed equally

BMC Medical Genetics 2007, 8:33doi:10.1186/1471-2350-8-33

Published:	12 June 2007

Abstract

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.