Abstract

Celiac disease (CD), one of the most common food intolerances worldwide, is characterized by small intestinal mucosal injury and malabsorption in genetically predisposed individuals. CD occurs in about 1% of the population and is triggered by the ingestion of storage proteins (i.e., gluten) found in wheat, rye, barley, and possibly oats. Biochemical studies on the structures of CD-toxic proteins and peptides and the genetic, molecular, and cellular mechanisms of CD have increased our understanding of CD pathogenesis considerably during the last two decades. Due to their high Gln and Pro contents, all CD-toxic proteins are resistant to complete proteolytic digestion by gastrointestinal enzymes. Consequently, large Pro- and Gln-rich peptides accumulate in the small intestine, reach the subepithelial lymphatic tissue, and induce two different immune responses in those with CD: a rapid innate response and slower adaptive response. Both responses result in mucosal destruction and epithelial apoptosis. Stimulat...

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