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neurogenetics

, Volume 13, Issue 1, pp 83–86 | Cite as

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

  • Christina M. Lill
  • Brit-Maren M. Schjeide
  • Denis A. Akkad
  • Paul Blaschke
  • Alexander Winkelmann
  • Lisa-Ann Gerdes
  • Sabine Hoffjan
  • Felix Luessi
  • Thomas Dörner
  • Shu-Chen Li
  • Elisabeth Steinhagen-Thiessen
  • Ulman Lindenberger
  • Andrew Chan
  • Hans-Peter Hartung
  • Orhan Aktas
  • Peter Lohse
  • Tania Kümpfel
  • Christian Kubisch
  • Joerg T. Epplen
  • Uwe K. Zettl
  • Lars Bertram
  • Frauke Zipp
Short Communication

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 Th17 lymphocytes in MS.

Keywords

STAT3 Multiple sclerosis Genetic association Replication 

Notes

Acknowledgements

We are grateful to the patients and control subjects who participated in this study. Furthermore, we thank all colleagues involved in the recruitment, examination and analyses of MS-free controls recruited as part of the “Berlin Aging Study II” (BASE-II), in particular Drs. Ilja Demuth, Rahel Eckardt, Hauke Heekeren, Martin Lövdén, Ludmilla Müller, Wilfried Nietfeld, Graham Pawelec, Florian Schmiedeck, Thomas Siedler and Gert G. Wagner. This project was funded by grants from the German Ministry for Education and Research (BMBF; to F.Z., L.B., U.K.Z. and U.L.), German Research Foundation (DFG; to F.Z.), the Cure Alzheimer's Fund (to L.B.), the Walter-and-Ilse-Rose-Stiftung (to H.-P.H. and O.A.) and the Innovation Fund of the Max Planck Society (to U.L.).

Competing interests

None.

References

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Copyright information

© Springer-Verlag 2011

Authors and Affiliations

  • Christina M. Lill
    • 1
    • 2
  • Brit-Maren M. Schjeide
    • 2
  • Denis A. Akkad
    • 3
  • Paul Blaschke
    • 4
  • Alexander Winkelmann
    • 4
  • Lisa-Ann Gerdes
    • 5
  • Sabine Hoffjan
    • 3
  • Felix Luessi
    • 1
  • Thomas Dörner
    • 6
  • Shu-Chen Li
    • 7
  • Elisabeth Steinhagen-Thiessen
    • 8
  • Ulman Lindenberger
    • 7
  • Andrew Chan
    • 9
  • Hans-Peter Hartung
    • 10
  • Orhan Aktas
    • 10
  • Peter Lohse
    • 11
  • Tania Kümpfel
    • 5
  • Christian Kubisch
    • 12
  • Joerg T. Epplen
    • 3
  • Uwe K. Zettl
    • 4
  • Lars Bertram
    • 2
    • 7
  • Frauke Zipp
    • 1
  1. 1.Department of NeurologyUniversity Medical Center of the Johannes Gutenberg-University MainzMainzGermany
  2. 2.Department of Vertebrate GenomicsMax Planck Institute for Molecular GeneticsBerlinGermany
  3. 3.Department of Human GeneticsRuhr UniversityBochumGermany
  4. 4.Department of NeurologyUniversity of RostockRostockGermany
  5. 5.Institute for Clinical NeuroimmunologyLudwig Maximilian UniversityMunichGermany
  6. 6.Department of Medicine, Rheumatology, and Clinical ImmunologyCharité University MedicineBerlinGermany
  7. 7.Max Planck Institute for Human DevelopmentBerlinGermany
  8. 8.Interdisciplinary Metabolic Center, Lipids ClinicCharité University MedicineBerlinGermany
  9. 9.Department of NeurologyRuhr UniversityBochumGermany
  10. 10.Department of Neurology, Medical FacultyHeinrich Heine UniversityDüsseldorfGermany
  11. 11.Department of Clinical ChemistryLudwig Maximilian UniversityMunichGermany
  12. 12.Institute of Human GeneticsUniversity of UlmUlmGermany

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