Celiac disease is an immune-mediated enteropathy triggered bythe ingestion of gluten-containing grains (including wheat,rye, and barley) in genetically susceptible persons. The diseaseis associated with HLA-DQ2 in 90 to 95 percent of cases andwith HLA-DQ8 in 5 to 10 percent of cases and is self-perpetuatingin the continued presence of gluten.1 It is the interplay betweengenes (both HLA and other types) and environment (i.e., gluten)that leads to the intestinal damage that is typical of the disease.2Under physiologic circumstances, this interplay is preventedby competent intercellular tight junctions, structures thatlimit the passage of macromolecules . . . [Full Text of this Article]
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From the Center for Celiac Research and Mucosal Biology Research Center, University of Maryland School of Medicine, Baltimore.
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