Coeliac disease (CD), the most common food sensitive enteropathy in humans, is caused by permanent intolerance for dietary gluten.1 2 Typical symptoms include chronic diarrhoea, abdominal distension, and failure to thrive. These symptoms are the result of a lesion in the upper small bowel characterised by (sub)total villous atrophy, hypertrophic crypts, an increased number of interepithelial lymphocytes, and a chronic inflammatory response of the lamina propria lymphocytes. IgA antibodies against endomysium are specific indicators of CD.3 4 Yet CD is considered to be primarily a T cell mediated disease because the majority of patients express the HLA-DQ2 [DQ(α1*0501, β1*02)], and/or −DQ8 [DQ(α1*03, β1*0302)] molecules5 6; gluten specific HLA-DQ restricted T cells are present at the site of the lesion in the gut7 and withdrawal of gluten stops the disease process.2 The identity of potentially disease inducing, gluten derived T cell stimulatory peptides, however, was unknown until recently.

Here we briefly discuss recent work which sheds light on the requirements for an optimal interaction between gluten, HLA-DQ, and T cells, requirements which explain the association of CD with HLA-DQ2/8.