TNF-α and IL10 polymorphisms interaction increases the risk of ankylosing spondylitis in Chinese Han population

Int J Clin Exp Pathol. 2015 Nov 1;8(11):15204-9. eCollection 2015.

Abstract

Aims: The target of this article was to reveal the role of tumor necrosis factors α (TNF-α) and Interleukin-10 (IL10) gene polymorphisms in ankylosing spondylitis (AS) development and explore the interaction between these two gene polymorphisms.

Methods: The genotyping of gene polymorphims was conducted using ABI Taqman assay method in 84 AS patients and 92 healthy people. Hardy-Weinberg equilibrium (HWE) was checked in the control group and the genotypes and alleles difference were compared with χ(2) test. Odds ratio (OR) with 95% confidence interval (CI) was calculated to identify the strength of association between gene polymorphism and disease. Meanwhile, multifactor dimensionality reduction (MDR) method was used to analysis the interaction between gene polymorphisms.

Results: The genotypes CG+CC of the minor allele in IL10 rs1878672 in cases was obviously higher frequency than the controls (P=0.03) and the minor allele C was also associated with the increased risk of AS, compared with G allele (OR=2.05, 95% CI=1.08-3.89). Rs3024490 in IL10 also showed a significant correlation to the onset risk of AS (GG vs. TT: OR=3.03, 95% CI=1.04-8.87; G vs. T: OR=1.70, 95% CI=1.08-2.68). What's more, there was the interaction between TNF-α rs3093662 and IL10 rs3021094, rs3024490 polymorphisms in AS.

Conclusions: IL10 rs1878672 and rs3024490 polymorphisms obviously increase the susceptibility to AS, but not TNF-α rs3093662. Both IL10 and TNF-α polymorphisms may affect the onset of AS.

Keywords: IL10; TNF-α; ankylosing spondylitis; interaction; polymorphism.

MeSH terms

  • Adolescent
  • Adult
  • Asian People / genetics*
  • Case-Control Studies
  • Female
  • Genetic Predisposition to Disease / genetics*
  • Genotype
  • Humans
  • Interleukin-10 / genetics*
  • Male
  • Polymorphism, Single Nucleotide*
  • Spondylitis, Ankylosing / genetics*
  • Tumor Necrosis Factor-alpha / genetics*

Substances

  • IL10 protein, human
  • Tumor Necrosis Factor-alpha
  • Interleukin-10