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Gliadin-Induced Zonulin Release and Autoimmunity in Celiac Disease | Mechanism Explained #3001470 (License: Personal Use)
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This detailed schematic shows the molecular cascade initiated by gliadin digestion: CXCR3-mediated zonulin release (step 2), PAR₂-dependent EGFR transactivation (step 3), and subsequent HLA-DQ/DR presentation of gliadin peptides (step 5), leading to Th1/Th17 polarization and T-cell migration to gut/pancreatic lymph nodes (step 6). Inflammation (step 7) and β-cell disruption (step 8) follow, with AT1001 (larazotide) blocking zonulin to prevent autoimmunity. The lower panel integrates histological evidence (villous atrophy, β-cell loss) with immune cell interactions (dendritic cells, macrophages, CD4⁺/CD8⁺ T cells).
Used in medical education, gastroenterology research pages, or patient-facing celiac disease resources to explain disease pathogenesis; matches user intent seeking mechanistic understanding of gluten intolerance, zonulin’s role, or therapeutic targets like larazotide.
Related Cliparts: Discover how gliadin fragments trigger zonulin release, increase gut permeability, and initiate autoimmune responses in celiac disease-key pathophysiological insights.
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