No support for a truncated interferon-α17 allele as risk factor for MS
Authors: Nyström, M.1; Ruuth, K.2; Lundgren, E.2; Sundström, P.1
Source: European Journal of Neurology, Volume 14, Number 11, November 2007 , pp. 1302-1304(3)
Publisher: Wiley-Blackwell
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.Keywords: candidate gene; interferon-α; multiple sclerosis; polymorphism
Document Type: Short communication
DOI: http://dx.doi.org/10.1111/j.1468-1331.2007.01953.x
Affiliations: 1: Department of Clinical Neuroscience, Umeå University, Umeå, Sweden; 2: Department of Molecular Biology, Umeå University, Umeå, Sweden
Publication date: 2007-11-01
- In this: publication
- By this: publisher
- In this Subject: Neurology & Psychiatry , Public Health
- By this author: Nyström, M. ; Ruuth, K. ; Lundgren, E. ; Sundström, P.

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