Intraluminal p31-43 gliadin peptide induces enteropathy

ARAYA R; JURY J; VERDU E; CHIRDO F

Nantes

Simposio; 28th Meeting of the European Prolamin Working Group of Prolamin Analysis and Toxicity; 2014

European Prolamin Working Group of Prolamin Analysis and Toxicity

Coeliac disease (CD) pathogenesis depends on the activation of gluten specific Th1 cells in susceptible individuals, who carry the HLA-DQ2 and/or HLA-DQ8 predisposing alleles [1,2]. The mechanisms, involved in the exacerbated expansion of Th1 cells, have been largely characterized during the last decades. Most of our knowledge of CD pathogenesis was based on the evaluation of small pieces of duodenal biopsies, which account for chronic lesions. Consequently, the initial steps of the mucosal damage are poorly understood [3]. Animal models are very useful tools to evaluate different steps in disease mechanisms and test new therapeutic strategies. Different complex models using genetically modified mice have been reported to assess CD pathogenesis [4]. The usefulness of different proposed animal models resides in mimicking certain steps of disease pathogenesis. Most studies focused on the analysis of the chronic phase of the disease, but few have evaluated the initial steps leading to mucosal damage or the precipitating factors of the disease. The aim of this work was to develop an animal model that mimic the initial steps of the CD pathogenesis