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Variation in ICOSLG influences Crohn's disease susceptibility
  1. Paul Henderson1,2,
  2. Johan van Limbergen1,3,4,
  3. Niall H Anderson5,
  4. Elaine R Nimmo2,
  5. Richard K Russell6,
  6. Jack Satsangi2,
  7. David C Wilson1,7
  1. 1Department of Child Life and Health, University of Edinburgh, Edinburgh, UK
  2. 2Gastrointestinal Unit, Centre for Molecular Medicine, University of Edinburgh, Edinburgh, UK
  3. 3Department of Paediatric Gastroenterology, Hepatology and Nutrition, Hospital for Sick Children, Toronto, Canada
  4. 4Department of Immunology, University of Toronto, Toronto, Canada
  5. 5Centre for Population Health Sciences, University of Edinburgh, Edinburgh, UK
  6. 6Department of Paediatric Gastroenterology, Royal Hospital for Sick Children, Yorkhill, Glasgow, UK
  7. 7Department of Paediatric Gastroenterology, Hepatology and Nutrition, Royal Hospital for Sick Children, Edinburgh, UK
  1. Correspondence to Paul Henderson, Department of Child Life and Health, University of Edinburgh, 20 Sylvan Place, Edinburgh EH9 1UW, UK; paul.henderson2{at}nhs.net

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Recent genome-wide association studies have identified more than 70 loci which confer susceptibility to Crohn's disease (CD).1 However, the critical coding regions within most of these loci are largely unidentified and it is therefore important that further work is carried out to robustly identify the candidate genes to guide future deep sequencing studies. A locus on chromosome 21q22 harbouring several genes including inducible T cell costimulator (ICOSLG), autoimmune regulator (AIRE) and periodic tryptophan protein 2 homologue (PWP2) has been shown to influence susceptibility to both adult and paediatric CD and ulcerative colitis (UC).1 2 The protein encoded by ICOSLG is intimately involved in the proliferation and differentiation of T lymphocytes (through binding with inducible T-cell costimulator (ICOS)), especially with regard to the balance between regulatory and Th17 subsets.

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