The cause of coeliac disease remained an enigma until the early 1950s when the Dutch paediatrician, W K Dicke made his seminal observation that gluten, the major storage protein of wheat cereal, is essential to the pathogenesis of the disease.1 Removal of gluten from the diet permits virtually complete recovery of the intestinal mucosa and reversal of the clinical and laboratory abnormalities. The precise mechanism whereby gluten causes damage to certain susceptible individuals has still to be elucidated. Many features of the disorder are in keeping with central involvement of the immune response, displaying a delayed-type hypersensitivity reaction to gluten. However, other features are in keeping with a so called autoimmune disease: these include a notable association with MHC class II genes (in particular HLA-DQ2), a female preponderance of approximately 3 to 1, and the presence of an autoantibody, the anti-endomysial antibody. Thus, coeliac disease could represent an unique example of autoimmune disease, where the disease process is absolutely dependent on continued exposure to an exogenous, dietary protein.

In 1983, Chorzelski and colleagues reported the association between gluten sensitive disease and circulating IgA anti-endomysial antibodies.2 In 1997, the nature of the endomysial antigen was discovered to be tissue transglutaminase3 and this gave an intriguing insight into the link between gluten and anti-endomysial …