Which sequence best summarizes the pathogenic mechanism by which celiac disease causes malabsorption after gluten exposure?

Ingestion of gluten → presentation of deamidated gluten peptides by HLA‑DQ2/8 → activation of T cells → immune-mediated damage to villi → villous atrophy → reduced absorptive surface and malabsorption.

Ingestion of gluten → direct enzymatic destruction of brush-border enzymes by gluten proteases → loss of microvilli without immune activation → selective carbohydrate malabsorption only, leaving fat and protein absorption intact.

Ingestion of gluten → colonization of the small intestine by gluten‑specialist bacteria that outcompete epithelial cells → synthesis of toxic short-chain fatty acids that dissolve villi → transient malabsorption reversible within days of gluten removal in all patients.

Ingestion of gluten → immediate IgE-mediated mast cell degranulation in the stomach → parietal cell destruction → achlorhydria and global intestinal villous hyperplasia that paradoxically increases stool output but improves micronutrient absorption.