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Independent replication of STAT3 association with multiple sclerosis risk in a large German case-control sample

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Lill,  C. M.
Neuropsychiatric Genetics (Lars Bertram), Dept. of Vertebrate Genomics (Head: Hans Lehrach), Max Planck Institute for Molecular Genetics, Max Planck Society;

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Schjeide,  B. M.
Neuropsychiatric Genetics (Lars Bertram), Dept. of Vertebrate Genomics (Head: Hans Lehrach), Max Planck Institute for Molecular Genetics, Max Planck Society;

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Bertram,  L.
Neuropsychiatric Genetics (Lars Bertram), Dept. of Vertebrate Genomics (Head: Hans Lehrach), Max Planck Institute for Molecular Genetics, Max Planck Society;

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Citation

Lill, C. M., Schjeide, B. M., Akkad, D. A., Blaschke, P., Winkelmann, A., Gerdes, L. A., et al. (2012). Independent replication of STAT3 association with multiple sclerosis risk in a large German case-control sample. Neurogenetics, 13(1), 83-6. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/22095036 http://www.springerlink.com/content/r9514vw301856238/fulltext.pdf.


Cite as: https://hdl.handle.net/11858/00-001M-0000-0010-7761-D
Abstract
Recent genome-wide association studies have implicated the "signal transducer and activator of transcription 3" gene (STAT3) as a putative new multiple sclerosis (MS) susceptibility locus. However, independent validation studies are sparse. Therefore, we performed a genetic association study of two STAT3 polymorphisms (rs744166 and rs2293152) in a large and independent German case-control sample of 5,904 subjects. We observed a nominally significant, albeit weak association between rs744166 and MS susceptibility (odds ratio = 1.09, P = 0.012) in our sample. This study supports the association between STAT3 and an increase in MS risk. Taking into account the functional role of STAT3, our results favour an involvement of T(h)17 lymphocytes in MS.