No support for a truncated interferon-alpha 17 allele as risk factor for MS
M Nyström1, K Ruuth, E Lundgren
1Department of Clinical Neuroscience, Umeå University, Umeå, Sweden.
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.
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