Coeliac disease is an inflammatory disease of the small intestine, precipitated in susceptible individuals by gliadin, the alcohol soluble (prolamin) fraction of wheat gluten. There is a strong genetic influence on susceptibility to develop coeliac disease. Ninety to ninety-five percent of patients are HLA-DQ2 positive which is coded by DQA1*0501 and DQB 1*0201 genes either in cis or in trans. The disease is characterised by crypt hyperplasia, villous atrophy and increased inflammatory cells in the epithelium and lamina propria. The pathogenesis is currently explained by the immunological hypothesis, which proposes that coeliac disease is being driven by an abnormal T cell response to gliadin. The enzyme tissue transglutaminase enhances T cell recognition of gliadin. In addition to gliadin, similar prolamin fractions of barley and rye (hordein and secalin respectively) are thought to activate the disease process. The safety of oats and its prolamin avenin is more controversial.

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