The association of particular major histocompatibility complex (MHC) polymorphisms with susceptibility to a number of autoimmune disease has been a puzzling phenomenon. This paper proposes a mechanism that might account in part for the onset of coeliac disease. Transaminase-mediated deamination of glutamine residues in gluten peptides may cause them to bind more tightly to disease-associated MHC alleles, activating heteroclitic gluten-peptide specific T-cell autoreactivity in the gut.
- Zaruhi Hovhannisyan
- Angela Weiss
- Bana Jabri
