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IL23R Arg381Gln is associated with childhood onset inflammatory bowel disease in Scotland
  1. J Van Limbergen1,
  2. %R K Russell2,
  3. E R Nimmo3,
  4. H E Drummond3,
  5. L Smith3,
  6. G Davies3,
  7. N H Anderson4,
  8. P M Gillett5,
  9. P McGrogan6,
  10. K Hassan6,
  11. L Weaver7,
  12. W M Bisset8,
  13. G Mahdi8,
  14. D C Wilson8,
  15. J Satsangi10
  1. 1Gastrointestinal Unit, Molecular Medicine Centre, Western General Hospital, University of Edinburgh, and Department of Paediatric Gastroenterology and Nutrition, Royal Hospital for Sick Children, Edinburgh, UK
  2. 2Department of Paediatric Gastroenterology and Nutrition, Royal Hospital for Sick Children, Edinburgh, UK
  3. 3Gastrointestinal Unit, Molecular Medicine Centre, Western General Hospital, University of Edinburgh, Edinburgh, UK
  4. 4Public Health Sciences, University of Edinburgh, Edinburgh, UK
  5. 5Department of Paediatric Gastroenterology and Nutrition, Royal Hospital for Sick Children, Edinburgh, UK
  6. 6Department of Paediatric Gastroenterology, Yorkhill Hospital, Glasgow, UK
  7. 7Department of Child Health, University of Glasgow, Glasgow, UK
  8. 8Department of Paediatric Gastroenterology, Royal Aberdeen Children’s Hospital, Aberdeen, UK
  9. 9Department of Paediatric Gastroenterology and Nutrition, Royal Hospital for Sick Children, Edinburgh, and Child Life and Health, University of Edinburgh, Edinburgh, UK
  10. 10Gastrointestinal Unit, Molecular Medicine Centre, Western General Hospital, University of Edinburgh, Edinburgh, UK
  1. Correspondence to:
    Dr Johan Van Limbergen
    Molecular Medicine Centre, Western General Hospital, Crewe Road, Edinburgh EH4 2XU, UK; johanvanlimbergen{at}hotmail.com

https://doi.org/10.1136/gut.2007.122069

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    The discovery of NOD2/CARD15 as the first susceptibility gene in Crohn’s disease has contributed significantly to a fundamental change in the direction of basic research in inflammatory bowel disease (IBD), triggering renewed interest in the integrity of the innate immune response in IBD and appropriate orchestration of a subsequent adaptive immune response.1,2 More widely, in all complex diseases this finding in 2001 provided a much welcomed and needed proof of principle for non-parametric linkage analysis.

    Another study with major implications for the pathogenesis of Crohn’s disease as well as for investigation of all complex disorders has recently been published.3 The North American consortium performed an association study testing 308 332 markers spanning the entire genome in 567 patients with ileal Crohn’s disease and 571 controls of non-Jewish European ancestry. Of the three markers reported to retain significance after stringent Bonferroni correction, two were located in the NOD2/CARD15 gene. The third marker (rs11209026) was a non-synonymous variant in the interleukin-23 receptor (IL23R) gene on chromosome 1p31. Replication was obtained in the index paper in a Jewish ancestry case-control analysis of patients with Crohn’s disease by transmission disequilibrium testing in 883 families with offspring affected by IBD and in a combined case-control analysis …

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    Footnotes

    • JVL is funded by a Research Training Fellowship from Action Medical Research, The Gay-Ramsay-Steel-Maitland or Stafford Trust and the Hazel M Wood Charitable Trust; RKR was funded by a University of Edinburgh Medical Faculty Fellowship and ERN is supported by a Wellcome Trust Programme Grant (072789/Z/03/Z). Financial assistance was also provided by Schering-Plough and the GI/Nutrition Research Fund, Child Life and Health, University of Edinburgh.

    • Competing interests: None.