title: The molecular basis for oat intolerance in patients with celiac disease.
abstract: BACKGROUND
  Celiac disease is a small intestinal inflammatory disorder characterized by malabsorption, nutrient deficiency, and a range of clinical manifestations. It is caused by an inappropriate immune response to dietary gluten and is treated with a gluten-free diet. Recent feeding studies have indicated oats to be safe for celiac disease patients, and oats are now often included in the celiac disease diet. This study aimed to investigate whether oat intolerance exists in celiac disease and to characterize the cells and processes underlying this intolerance.
  
  
  RESULTS
  We selected for study nine adults with celiac disease who had a history of oats exposure. Four of the patients had clinical symptoms on an oats-containing diet, and three of these four patients had intestinal inflammation typical of celiac disease at the time of oats exposure. We established oats-avenin-specific and -reactive intestinal T-cell lines from these three patients, as well as from two other patients who appeared to tolerate oats. The avenin-reactive T-cell lines recognized avenin peptides in the context of HLA-DQ2. These peptides have sequences rich in proline and glutamine residues closely resembling wheat gluten epitopes. Deamidation (glutamine-->glutamic acid conversion) by tissue transglutaminase was involved in the avenin epitope formation.
  
  
  CONCLUSIONS
  We conclude that some celiac disease patients have avenin-reactive mucosal T-cells that can cause mucosal inflammation. Oat intolerance may be a reason for villous atrophy and inflammation in patients with celiac disease who are eating oats but otherwise are adhering to a strict gluten-free diet. Clinical follow-up of celiac disease patients eating oats is advisable.
authors.affiliation: Institute of Immunology, Rikshospitalet University Hospital, University of Oslo, Oslo, Norway.
authors.forename: Helene
authors.initials: H
authors.lastname: Arentz-Hansen
authors.forename: Burkhard
authors.initials: B
authors.lastname: Fleckenstein
authors.forename: Øyvind
authors.initials: Ø
authors.lastname: Molberg
authors.forename: Helge
authors.initials: H
authors.lastname: Scott
authors.forename: Frits
authors.initials: F
authors.lastname: Koning
authors.forename: Günther
authors.initials: G
authors.lastname: Jung
authors.forename: Peter
authors.initials: P
authors.lastname: Roepstorff
authors.forename: Knut E A
authors.initials: KE
authors.lastname: Lundin
authors.forename: Ludvig M
authors.initials: LM
authors.lastname: Sollid
mesh_terms: D001284:Atrophy; D018554:Avena; D002446:Celiac Disease / Q000503:physiopathology*; D004032:Diet; D006801:Humans; D007249:Inflammation; D007413:Intestinal Mucosa / Q000276:immunology* / Q000473:pathology; D010940:Plant Proteins / Q000276:immunology; D055315:Prolamins; D013601:T-Lymphocytes / Q000276:immunology*
chemical_list: D010940:Plant Proteins; D055315:Prolamins