Coeliac disease is a gut disease driven by an abnormal immune response towards dietary gluten in genetically susceptible individuals. Whether and, if so, how abnormal transport of gluten across the gut epithelium may participate in the pathogenesis of coeliac disease remains debatable. This paper summarises the interactions of gluten-derived peptides with the intestinal epithelium and discusses the mechanisms that control their transport across the epithelium. It shows how recent data point to a key role for the transcellular pathway and highlights the 'Trojan horse' role of secretory IgA which can hijack the transferrin receptor and allow the rapid translocation of intact gluten peptides into the mucosa. These recent findings might be useful for the design of new treatments.