Investigating the molecular basis for specific and cross-reactive T cell responses in Celiac Disease

Celiac disease is triggered by ingestion of gluten from wheat, rye and barley in genetically susceptible patients. In the western population, only 1% of individuals develop celiac disease despite 35% being genetically predisposed. This suggests that environmental exposure plays a role in aetiology of disease. This thesis links bacterial exposure with celiac disease as patients could recognise molecular mimics of gluten derived from Pseudomonas species. We uncovered the mechanism behind immune cell recognition of wheat-gluten peptides and bacterially-derived molecular mimics of these peptides. Future efforts to target key interactions identified in this study may offer therapeutic benefit.