Association of a CD24 gene polymorphism with susceptibility to systemic lupus erythematosus

Arthritis Rheum. 2007 Sep;56(9):3080-6. doi: 10.1002/art.22871.

Abstract

Objective: To determine the potential role of the CD24 A57V gene polymorphism in systemic lupus erythematosus (SLE).

Methods: We studied 3 cohorts of Caucasian patients and controls. The Spanish cohort included 696 SLE patients and 539 controls, the German cohort included 257 SLE patients and 317 controls, and the Swedish cohort included 310 SLE patients and 247 controls. The CD24 A57V polymorphism was genotyped by polymerase chain reaction, using a predeveloped TaqMan allele discrimination assay. Odds ratios (ORs) and 95% confidence intervals (95% CIs) were calculated.

Results: In the Spanish cohort there was a statistically significant difference in the distribution of the CD24 V allele between SLE patients and controls (OR 3.6 [95% CI 2.13-6.16], P < 0.0001). In addition, frequency of the CD24 V/V genotype was increased in SLE patients compared with controls (OR 3.7 [95% CI 2.16-6.34], P < 0.00001). We sought to replicate this association with SLE in a German population and a Swedish population. A similar trend was found in the German group. The CD24 V/V genotype and the CD24 V allele were more frequent in SLE patients than in controls, although this difference was not statistically significant. No differences were observed in the Swedish group. A meta-analysis of the Spanish and German cohorts demonstrated that the CD24 V allele has a risk effect in SLE patients (pooled OR 1.25 [95% CI 1.08-1.46], P = 0.003). In addition, homozygosity for the CD24 V risk allele significantly increased the effect (pooled OR 2.19 [95% CI 1.50-3.22], P = 0.00007).

Conclusion: These findings suggest that the CD24 A57V polymorphism plays a role in susceptibility to SLE in a Spanish population.

Publication types

  • Multicenter Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • CD24 Antigen / genetics*
  • Cohort Studies
  • Female
  • Genetic Predisposition to Disease*
  • Humans
  • Lupus Erythematosus, Systemic / genetics*
  • Male
  • Polymorphism, Genetic*

Substances

  • CD24 Antigen