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FRANCISCO AGUILAR, ANTONIO NÚÑEZ-ROLDÁN, BELÉN TORRES, INGEBORG WICHMANN, JULIO SÁNCHEZ-ROMÁN, and MARIA FRANCISCA GONZÁLEZ-ESCRIBANO

ABSTRACT.

Objective. To investigate the possible association of CCR2 and CCR5 chemokine receptor gene polymorphisms with the susceptibility, clinical features, and the outcome of systemic lupus erythematosus (SLE).

Methods. We studied 276 patients with SLE and 194 ethnically matched healthy controls. Patients were stratified according to their clinical features and outcome. Genotyping of 190 (A/G) CCR2 and D32CCR5 was performed using polymerase chain reaction techniques.

Results. No association between the polymorphisms studied and susceptibility to SLE was found. However, when patients were stratified according to their clinical features, an increase in the frequency of individuals bearing D32CCR5 among patients with anti-dsDNA antibodies was found [15.1% vs 6.4% in negative patients (p = 0.03, p_corr > 0.05, OR 2.61, 95% CI 1.04–7.40) and 8% in controls (p = 0.04, p_corr > 0.05, OR 1.97, 95% CI 0.97–4.11)]. Moreover, a significant increase in the frequency of D32CCR5 individuals was observed among patients with biopsy-proven nephritis [20.5% vs 8.5% in patients without nephritis (p = 0.03, p_corr > 0.05, OR 2.79, 95% CI 0.93–7.70) and 8% in controls (p_Fisher = 0.04, p_corr > 0.05, OR 2.87, 95% CI 0.97–7.82)]. Regarding the outcome, a higher median severity index was found among patients bearing D32CCR5 (33.5 ± 17.9 vs 26.6 ± 17.1 in CCR5/CCR5 individuals; p = 0.04).

Conclusion. Polymorphisms of CCR2 and CCR5 do not seem to be involved in susceptibility to SLE, although a slight contribution of the CCR5 polymorphism in the production of anti-dsDNA autoantibodies, in the development of lupus nephritis, and in the outcome of the disease could be postulated. (J Rheumatol 2003;30:1770-4)

Key Indexing Terms:

CCR2
CCR5
SYSTEMIC LUPUS ERYTHEMATOSUS
GENETIC POLYMORPHISM

Supported in part by grants from Fondo de Investigaciones Sanitarias (FIS 00/0566), Plan Andaluz de Investigación (PAI, grupo CTS-0197), and Fundación Reina Mercedes. Dr. Aguilar is the recipient of a fellowship from Fondo de Investigaciones Sanitarias (FIS 00/0566) and Dr. Torres is the recipient of a fellowship from Fundación Reina Mercedes.

F. Aguilar, PhD; A. Núñez-Roldán, MD, PhD; B. Torres, PhD; I. Wichmann, MD, PhD; J. Sánchez-Román, MD, PhD; M.F. González-Escribano, PhD.

Address reprint requests to Dr. A. Núñez-Roldán, Servicio de Inmunología, Hospital Universitario Virgen del Rocío, 41013 Sevilla, Spain. E-mail: antonio.nunez.sspa@juntadeandalucia.es

Submitted July 24, 2002; revision accepted January 23, 2003.