MHC2TA and FCRL3 genes are not associated with rheumatoid arthritis in Mexican patients

Rheumatol Int. 2016 Feb;36(2):249-54. doi: 10.1007/s00296-015-3358-2. Epub 2015 Sep 8.

Abstract

Rheumatoid arthritis (RA) is a multifactorial disease. A combination of genetic and environmental risk factors contributes to its etiology. Several genes have been reported to be associated with susceptibility to the development of RA. The MHC2TA and FCRL3 genes have been associated previously with RA in Swedish and Japanese populations, respectively. In two recent reports, we show an association between FCRL3 and juvenile rheumatoid arthritis (JRA), and MHC2TA and acute coronary syndrome (ACS) in Mexican population. We assessed the association between three single nucleotide polymorphisms (SNPs) of the MHC2TA (-168G/A; rs3087456, and +16G/C; rs4774) and FCRL3 (-169T/C; rs7528684) genes and rheumatoid arthritis in Mexican population through a genotyping method using allelic discrimination assays with TaqMan probes. Our case-control study included 249 patients with RA and 314 controls. We found no evidence of an association between the MHC2TA -168G/A and +1614G/C or FCRL3 -169T/C polymorphisms and RA in this Mexican population. In this cohort of Mexican patients with RA, we observed no association between the MHC2TA or FCRL3 genes and this autoimmune disease.

Keywords: FCRL3; MHC2TA; Polymorphism; Rheumatoid arthritis.

MeSH terms

  • Adult
  • Arthritis, Rheumatoid / diagnosis
  • Arthritis, Rheumatoid / epidemiology
  • Arthritis, Rheumatoid / genetics*
  • Case-Control Studies
  • Female
  • Gene Frequency
  • Genetic Association Studies
  • Genetic Predisposition to Disease
  • Haplotypes
  • Humans
  • Male
  • Mexico / epidemiology
  • Middle Aged
  • Nuclear Proteins / genetics*
  • Phenotype
  • Polymorphism, Single Nucleotide*
  • Receptors, Immunologic / genetics*
  • Risk Factors
  • Trans-Activators / genetics*

Substances

  • FCRL3 protein, human
  • MHC class II transactivator protein
  • Nuclear Proteins
  • Receptors, Immunologic
  • Trans-Activators