title: No support for a truncated interferon-alpha 17 allele as risk factor for MS.
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.
authors.affiliation: Department of Clinical Neuroscience, Umeå University, Umeå, Sweden.
authors.forename: M
authors.initials: M
authors.lastname: Nyström
authors.forename: K
authors.initials: K
authors.lastname: Ruuth
authors.forename: E
authors.initials: E
authors.lastname: Lundgren
authors.forename: P
authors.initials: P
authors.lastname: Sundström
mesh_terms: D000483:Alleles; D006801:Humans; D016898:Interferon-alpha / Q000235:genetics*; D009103:Multiple Sclerosis / Q000235:genetics*; D011110:Polymorphism, Genetic / Q000235:genetics; D012307:Risk Factors
chemical_list: C471357:IFNA17 protein, human; D016898:Interferon-alpha