[Polymorphism of Fc gamma RIIIA-158F/V gene and promoter region of IL-10 gene in systemic lupus erythematosus in Kazakhs]

Ter Arkh. 2003;75(5):36-41.
[Article in Russian]

Abstract

Aim: To assess the role of allele polymorphism of genes Fc gamma RIII and IL-10 in systemic lupus erythematosus (SLR) in a homogeneous (stratified by nationality) Kazakh population sample.

Material and methods: Polymorphism of genes Fc gamma RIIIA and IL-10 was studied in 49 patients SLE patients and 81 healthy subjects (control group). Detection of two allele variants of gene Fc gamma RIIIA (alleles F and V) caused by point mutation in position 559 was performed by polymerase chain reaction (PCR) in the amplification refractory mutation system. Genetic changeability of IL-10 gene promotion site due to point mutation in position 627 (alleles 1 and 2) was investigated by polymorphism of restricted fragment lengths using restrictase RsaI.

Results: Significant differences in the distribution rates of genes Fc gamma RIIIA and IL-10 were revealed in SLE patients versus controls. Alleles F and -627A (1), including homozygous ones, are genes predisposing to development of SLE while variants of the markers V and -627 (2) are protecting genes. If a SLE patient's genotype combines alleles F of gene Fc gamma RIII and alleles 1 of gene IL-10 (F/F + 1/1), this patient has an 8 times higher risk to develop SLE.

Conclusion: Polymorphism of genes Fc gamma RIIIA and IL-10 is associated with predisposition to development of SLE in Kazakh population. The analysis of combined genotypes of the studied genes suggests a synergic action of genes Fc gamma RIIIA and IL-10 on the risk to develop SLE.

Publication types

  • Comparative Study
  • English Abstract

MeSH terms

  • Adult
  • Alleles
  • Female
  • Genetic Predisposition to Disease
  • Genotype
  • Homozygote
  • Humans
  • Interleukin-10 / genetics*
  • Kazakhstan
  • Lupus Erythematosus, Systemic / genetics*
  • Lupus Erythematosus, Systemic / immunology
  • Male
  • Middle Aged
  • Point Mutation
  • Polymerase Chain Reaction
  • Polymorphism, Genetic*
  • Promoter Regions, Genetic
  • Receptors, IgG / genetics*
  • Risk Factors

Substances

  • Receptors, IgG
  • Interleukin-10