Lack of association between the chemokine receptor 5 polymorphism CCR5delta32 in rheumatoid arthritis and juvenile idiopathic arthritis.
| Autor: | Lindner E; Institute of Immunology, Rikshospitalet-Radiumhospitalet Medical Center, 0027 Oslo, Norway. Ewald.Lindner@student.uibk.ac.at, Nordang GB, Melum E, Flatø B, Selvaag AM, Thorsby E, Kvien TK, Førre OT, Lie BA |
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| Jazyk: | angličtina |
| Zdroj: | BMC medical genetics [BMC Med Genet] 2007 Jun 12; Vol. 8, pp. 33. Date of Electronic Publication: 2007 Jun 12. |
| DOI: | 10.1186/1471-2350-8-33 |
| Abstrakt: | 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 CCR5Delta32 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 CCR5Delta32 polymorphism is associated with RA or JIA in Norwegian cohorts. Methods: 853 RA patients, 524 JIA patients and 658 controls were genotyped for the CCR5Delta32 polymorphism. Results: The CCR5Delta32 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 CCR5Delta32, as previously suggested. Conclusion: Our data do not support an association between the CCR5Delta32 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 CCR5Delta32 in RA, albeit substantially weaker than the effect first reported. |
| Databáze: | MEDLINE |
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