Gluten-sensitive disease is activated in genetically susceptible individuals by the ingestion of wheat protein (gluten). Breakdown in normal tolerogenic processes to dietary gluten is likely to play a primary pathogenic role. The disease is characterized by several autoimmune-type features and provides a model for studying autoimmune processes. A recent meeting emphasized the need for a clearer picture of the molecular interactions between disease triggering agents, molecules of the immune system and other products of disease susceptibility genes.