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Paneth cell marker CD24 in NOD2 knockout organoids and in inflammatory bowel disease (IBD)
  1. Johan Van Limbergen1,2,
  2. Kaoru Geddes3,
  3. Paul Henderson2,
  4. Richard K Russell4,
  5. Hazel E Drummond5,
  6. Jack Satsangi5,
  7. Anne M Griffiths6,
  8. Dana J Philpott3,
  9. David C Wilson2
  1. 1Division of Gastroenterology and Nutrition, Department of Pediatrics, IBD Centre, Dalhousie University, Halifax, Nova Scotia, Canada
  2. 2Department of Child Life and Health, University of Edinburgh, Edinburgh, UK
  3. 3Department of Immunology, University of Toronto, Toronto, Ontario, Canada
  4. 4Department of Paediatric Gastroenterology, Yorkhill Hospital, Glasgow, UK
  5. 5Gastrointestinal Unit, University of Edinburgh, Edinburgh, UK
  6. 6Division of Paediatric Gastroenterology, Hospital for Sick Children, Toronto, Ontario, Canada
  1. Correspondence to  Dr Johan Van Limbergen, IBD Centre, Division of Gastroenterology & Nutrition, Department of Paediatrics, Dalhousie University, IWK Health Centre, 5850 University Avenue, Halifax, Nova Scotia, B3K 6R8, Canada; johanvanlimbergen{at}hotmail.com

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We read with great interest the article by Shanahan et al1 describing the roles of environmental conditions, notably co-housing with wild type (WT) littermates, and mouse genetic background in nucleotide-binding oligomerisation domain-containing protein 2 (NOD2)-dependent production of anti-microbial peptides in the mouse intestine. These authors demonstrate that expression, translation and anti-microbial activity of α-defensins are independent of NOD2.1 Robertson et al2 recently confirmed that housing conditions rather than NOD2 status influenced intestinal microbiota composition. Shanahan et al address the question whether an increase in the number of Paneth cells could compensate for a NOD2-dependent reduction in the level of defensin production in Paneth cells. Using a combination of hematoxylin and eosin staining (to assess crypt numbers), immunohistochemistry (using anti-lyzozyme staining) and flow cytometry (sorting for expression of lyzozyme and lack of expression of CD45—a haematopoietic cell marker) of the entire ilea of WT and NOD2-deficient mice showed NOD2 status did not influence Paneth cell numbers.1

CD24, a heavily glycosylated protein marker of intestinal crypt stem cells and Paneth cells, is upregulated in inflammatory bowel disease (IBD).3 ,4 Sato et al3 demonstrated that the combination of CD24hi and …

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