No support for a truncated interferon-alpha 17 allele as risk factor for MS

Eur J Neurol. 2007 Nov;14(11):1302-4. doi: 10.1111/j.1468-1331.2007.01953.x.

Abstract

Cytokines have a central role in multiple sclerosis (MS) pathogenesis and may contribute to the aetiology of MS. A polymorphism in the IFNA17 gene with an allele carrying a pre-mature stop codon has been suggested to convey a 26-fold increased risk for MS. We investigated the possible association between this polymorphism and MS using population-based samples from a genetically well-characterized population. The IFNA17 gene variant was found in 2.8% of 327 MS cases and 3.3% of 698 referents (P = 0.64). Thus, our study does not support an association between the IFNA17 allele and risk for MS.

MeSH terms

  • Alleles*
  • Humans
  • Interferon-alpha / genetics*
  • Multiple Sclerosis / genetics*
  • Polymorphism, Genetic / genetics
  • Risk Factors

Substances

  • IFNA17 protein, human
  • Interferon-alpha