La maladie cœliaque en 2009 : un futur sans régime ?

Abstract

Celiac disease is an enteropathy related to autoimmune diseases induced by gluten in genetically predisposed individuals. Its prevalence is of 1% in Europe and United States. Its clinical presentation is extremely various and diagnosis relies on the detection of specific serum antibodies and on the demonstration of intestinal villous atrophy. Treatment relies on a life-long gluten free diet which prevents bone, autoimmune and malignant complications. The keystone of its pathogenesis is the interaction of gliadin peptides with HLA DQ2/8 molecules, the main genetic risk factor, which induces the activation of CD4+ T-cells in the lamina propria. Yet, complementary mechanisms are necessary to provoke the loss of tolerance to gluten which involves the cytokine IL-15 responsible of the activation/expansion of intraepithelial lymphocytes, a hallmark of the origin of the severe lymphomatous complications. The burden of the gluten-free diet leads to a strong demand for alternative treatments. Numerous strategies have been identified to prevent the recognition of gliadin peptides by the immune system. Their efficiency and safety remained to be evaluated, the most attainable strategy today being oral therapy by enzymes able to eliminate gluten immunogenicity.