Polymorphisms in the promoter region of RANTES and the regulatory region of monocyte chemoattractant protein-1 among Chinese children with systemic lupus erythematosus

J Rheumatol. 2004 Oct;31(10):2062-7.

Abstract

Objective: Chemokines play an important role in the physiology and pathophysiology of acute and chronic inflammatory processes. We investigated whether chemokines such as RANTES (regulated upon activation, normally T cell expressed and secreted) promoter and monocyte chemoattractant protein-1 (MCP-1) regulatory polymorphisms were associated with systemic lupus erythematosus (SLE) in Chinese children.

Methods: Forty-six patients with SLE and 107 healthy children of comparable ages were studied for genotypes with polymerase chain reaction-based assays.

Results: The frequency and distribution of genotypes of the -28(C/G) RANTES gene polymorphism were significantly different between the 2 groups (p < 0.001), and the RANTES -28G allele was significantly more frequent in patients with SLE than in healthy controls (23.9% vs 11%; p = 0.006, OR 2.37, 95% CI 1.25-4.28). There was no significant difference in the frequency or in the distribution of genotypes of the -2518(A/G) MCP-1 and the -403(G/A) RANTES gene polymorphisms between patients and controls (p = 0.32 and p = 0.19, respectively). The RANTES -28G allele was also significantly associated with higher initial levels of antinuclear antibody, lower levels of C3, and higher incidences of central nervous system lupus.

Conclusion: In the Chinese population, children with RANTES -28C/G polymorphisms have increased risk of developing SLE. Healthy controls with the C/G or G/G genotype were 2.37 times more likely to have SLE compared to those with the C/C genotype.

MeSH terms

  • Adolescent
  • Chemokine CCL2 / genetics*
  • Chemokine CCL5 / genetics*
  • Child
  • China
  • Female
  • Gene Frequency
  • Genetic Predisposition to Disease
  • Genotype
  • Humans
  • Lupus Erythematosus, Systemic / genetics*
  • Lupus Erythematosus, Systemic / immunology
  • Male
  • Polymorphism, Genetic*
  • Promoter Regions, Genetic*
  • Regulatory Sequences, Nucleic Acid*

Substances

  • CCL2 protein, human
  • Chemokine CCL2
  • Chemokine CCL5