Interleukin-10 promoter polymorphisms in Southern Chinese patients with systemic lupus erythematosus

Arthritis Rheum. 1998 Jun;41(6):1090-5. doi: 10.1002/1529-0131(199806)41:6<1090::AID-ART16>3.0.CO;2-6.

Abstract

Objective: To study the genetic association of interleukin-10 (IL-10) promoter polymorphisms in Southern Chinese patients with systemic lupus erythematosus (SLE), and to investigate possible associations with clinical manifestations of the disease.

Methods: DNA was extracted from 88 Chinese patients with SLE and 83 ethnically matched controls. The IL-10 promoter region between positions -533 and -1120 was amplified by polymerase chain reaction, and polymorphisms were detected by restriction-enzyme cleavage.

Results: No significant difference in the allele or haplotype frequencies between SLE patients and controls could be demonstrated. The *A and *C alleles at the -597 position were linked to the *T and *C alleles at the -824 position, respectively. However, when clinical features were examined, the *A allele at the -597 position and the *T allele at the -824 position were significantly associated with lupus nephritis, by chi-square analysis (P < 0.001, odds ratio 4.19, 95% confidence interval 2.02-8.71). Similarly, the haplotype -1087*A/-824*T/-597*A was also associated with renal involvement (P < 0.001, odds ratio 3.62, 95% confidence interval 1.80-7.31).

Conclusion: IL-10 promoter polymorphisms are not strong determinants of susceptibility to the development of SLE, per se, in Southern Chinese individuals. However, IL-10 genotypes are strongly associated with certain clinical manifestations of SLE and may have a role in predicting disease prognosis.

MeSH terms

  • Adult
  • Asian People / genetics*
  • Autoantibodies / analysis
  • Autoantibodies / genetics
  • China / ethnology
  • Female
  • Genotype
  • Haplotypes / genetics
  • Humans
  • Interleukin-10 / genetics*
  • Lupus Erythematosus, Systemic / ethnology*
  • Lupus Erythematosus, Systemic / genetics*
  • Lupus Erythematosus, Systemic / physiopathology
  • Lupus Nephritis / genetics
  • Lupus Nephritis / physiopathology
  • Male
  • Polymorphism, Genetic / genetics*
  • Promoter Regions, Genetic / genetics*

Substances

  • Autoantibodies
  • Interleukin-10