RT Journal Article
SR Electronic
T1 Lack of Association of C-C Chemokine Receptor 5 Δ32 Deletion Status with Rheumatoid Arthritis, Systemic Lupus Erythematosus, Lupus Nephritis, and Disease Severity
JF The Journal of Rheumatology
JO J Rheumatol
FD The Journal of Rheumatology
SP jrheum.091468
DO 10.3899/jrheum.091468
A1 Henk A. Martens
A1 Sacha Gross
A1 Gerrit van der Steege
A1 Elisabeth Brouwer
A1 Jo H.M. Berden
A1 Ruud de Sevaux
A1 Ronald H.W.M. Derksen
A1 Alexandre E. Voskuyl
A1 Stefan P. Berger
A1 Gerjan J. Navis
A1 Cees G.M. Kallenberg
A1 Marc Bijl
YR 2010
UL http://www.jrheum.org/content/early/2010/07/29/jrheum.091468.abstract
AB Objective C-C chemokine receptor 5 (CCR5) plays an important role in inflammation. A 32 base-pair (∆32) deletion in the CCR5 gene leads to a nonfunctional receptor. This deletion has been reported to have a protective effect on the development and progression of several autoimmune diseases. We investigated whether the ∆32 deletion is associated with disease susceptibility in a population of patients with rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and lupus nephritis (LN); and whether it is associated with disease severity. Methods DNA samples from 405 RA patients, 97 SLE patients, 113 LN patients, and 431 healthy controls were genotyped for the CCR5 ∆32 deletion. Differences in genotype frequencies were tested between patients and controls. Association of genotypes with disease severity was analyzed. Results Genotype frequencies of each group were in Hardy-Weinberg equilibrium. The genotype frequencies of patients did not differ significantly from controls (CCR5/∆32, ∆32/∆32: RA 18.3% and 1.2%, respectively; SLE 17.5% and 2.1%; LN 13.3% and 1.8%; controls 20.0% and 2.8%). However, there was a trend for lower ∆32 deletion allele frequency in LN patients compared to controls (p = 0.08). There was no significant association between the CCR5 status and disease severity in RA, SLE, or LN. Conclusion Although an association with LN cannot be excluded, the CCR5 ∆32 deletion does not seem to be a disease susceptibility genotype for RA, SLE, or LN. No significant effect of the ∆32 deletion on disease severity was demonstrated.