In celiac disease (CD), abnormal immune-mediated responses follow ingestion of gluten. Although the triggering agent is a dietary protein, the disease has autoimmune components because of the presence of autoantibodies and its association with autoimmune conditions. We review the most recent studies on CD pathogenesis and the possibilities to modulate immune dysfunction in CD.
Keywords: epidermal growth factor, glutenins, anti-endomysium antibodies, tissue transglutaminase type II, prolyl endopeptidases
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