TY - JOUR 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 DO - 10.3899/jrheum.091468 SP - jrheum.091468 AU - Henk A. Martens AU - Sacha Gross AU - Gerrit van der Steege AU - Elisabeth Brouwer AU - Jo H.M. Berden AU - Ruud de Sevaux AU - Ronald H.W.M. Derksen AU - Alexandre E. Voskuyl AU - Stefan P. Berger AU - Gerjan J. Navis AU - Cees G.M. Kallenberg AU - Marc Bijl Y1 - 2010/08/03 UR - http://www.jrheum.org/content/early/2010/07/29/jrheum.091468.abstract N2 - 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. ER -