Ineke C M Lavrijsen

Publications (2)35.53 Total impact

• Source

  Available from: Erica van Oort

  Article: Myosin IXB variant increases the risk of celiac disease and points toward a primary intestinal barrier defect.

  Alienke J Monsuur, Paul I W de Bakker, Behrooz Z Alizadeh, Alexandra Zhernakova, Marianna R Bevova, Eric Strengman, Lude Franke, Ruben van't Slot, Martine J van Belzen, Ineke C M Lavrijsen, Begoña Diosdado, Mark J Daly, Chris J J Mulder, M Luisa Mearin, Jos W R Meijer, Gerrit A Meijer, Erica van Oort, Martin C Wapenaar, Bobby P C Koeleman, Cisca Wijmenga
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  ABSTRACT: Celiac disease is probably the best-understood immune-related disorder. The disease presents in the small intestine and results from the interplay between multiple genes and gluten, the triggering environmental factor. Although HLA class II genes explain 40% of the heritable risk, non-HLA genes accounting for most of the familial clustering have not yet been identified. Here we report significant and replicable association (P = 2.1 x 10(-6)) to a common variant located in intron 28 of the gene myosin IXB (MYO9B), which encodes an unconventional myosin molecule that has a role in actin remodeling of epithelial enterocytes. Individuals homozygous with respect to the at-risk allele have a 2.3-times higher risk of celiac disease (P = 1.55 x 10(-5)). This result is suggestive of a primary impairment of the intestinal barrier in the etiology of celiac disease, which may explain why immunogenic gluten peptides are able to pass through the epithelial barrier.
  Nature Genetics 01/2006; 37(12):1341-4. · 35.53 Impact Factor
• Article: Myosin IXB variant increases the risk of celiac disease and points toward a primary intestinal barrier defect

  Alienke J Monsuur, Paul I W de Bakker, Behrooz Z Alizadeh, Alexandra Zhernakova, Marianna R Bevova, Eric Strengman, Lude Franke, Ruben van't Slot, Martine J van Belzen, Ineke C M Lavrijsen, Bego|[ntilde]|a Diosdado, Mark J Daly, Chris J J Mulder, M Luisa Mearin, Jos W R Meijer, Gerrit A Meijer, Erica van Oort, Martin C Wapenaar, Bobby P C Koeleman, Cisca Wijmenga
  [show abstract] [hide abstract]
  ABSTRACT: Celiac disease is probably the best-understood immune-related disorder. The disease presents in the small intestine and results from the interplay between multiple genes and gluten, the triggering environmental factor1. Although HLA class II genes explain 40% of the heritable risk, non-HLA genes accounting for most of the familial clustering have not yet been identified. Here we report significant and replicable association (P = 2.1 10-6) to a common variant located in intron 28 of the gene myosin IXB (MYO9B), which encodes an unconventional myosin molecule that has a role in actin remodeling of epithelial enterocytes2, 3. Individuals homozygous with respect to the at-risk allele have a 2.3-times higher risk of celiac disease (P = 1.55 10-5). This result is suggestive of a primary impairment of the intestinal barrier in the etiology of celiac disease, which may explain why immunogenic gluten peptides are able to pass through the epithelial barrier.
  Nature Genetics. 11/2005; 37(12):1341-1344.