La maladie cœliaque: Une maladie auto-immune induite par un antig̀ene alimentaire

Coeliac disease is an autoimmune enteropathy induced by a dietary antigen, gliadin, in genetically predisposed individuals. The genetic linkage to HLADQ2/8 and the identification of the enzyme transglutaminase as the target for the autoantibodies have led to propound a key pathogenic role for lamina propria HLA-DQ2/8 restricted CD4+ T cells recognizing gliadin peptides deamidated by tranglutaminase. Autoantibody production is ascribed to the recognition of transglutaminase bound to gliadin by the immune system. The mechanism of the intraepithelial lymphoid hyperplasia, which is a hallmark of the disease and gives rise to malignant complications, remains elusive. It may be triggered by a toxic peptide distinct from the peptides stimulating the CD4 lymphocytes, and is likely favoured by the release of cytokines and activation of innate lymphocyte receptors by enterocytes modified by stress and inflammation. Identification of other genetic and environmental factors remains necessary to define the mechanisms triggering the abnormal immune response to gliadin, to understand the rationale for the wide clinical and histological spectrum, and in the long term to design alternative treatments to the current strenuous gluten free diet.