Coeliac disease (also gluten-sensitive enteropathy, GSE) is a systemic autoimmune disease in which genetic predisposition play a pronounced role. Coeliac disease may affect different organ systems. Its prevalence is estimated to be around 1 %, with experts assuming a large number of undiagnosed cases due to atypical or mild symptoms. Coeliac disease mostly manifests as a severe inflammation and damage of the mucosa of the small intestine (enteropathy). In conjunction with the resulting disruption of the nutrient absorption, a wide range of clinical gastrointestinal and non-gastrointestinal symptoms (among others chronic diarrhoea, abdominal pain, weight loss), can be observed. The clinical picture of coeliac disease may also include a chronic rash in the form of Duhring’s dermatitis.

Coeliac disease is caused by an overreaction of the immune system following ingestion of gluten, especially of the so-called gliadin, which accounts for around 90 % of the protein content of many grains. Gliadin can be only partially digested in the small intestine. If the intestinal epithelium presents gaps, as typically occurs in patients with coeliac disease, gliadin fragments may pass the intestinal barrier and reach the underlying connective tissue. There, the enzyme tissue transglutaminase (tTG) deamidates the amino acid glutamine into glutamic acid at specific loci of the gliadin peptides. Given a genetic predisposition, this modification causes the peptides to have an immunological effect. Activation of the B cells leads to the formation of antibodies against the deamidated gliadin peptides (DGP) and the body-own tTG. Furthermore, T-cells secrete proinflammatory cytokines, which cause inflammatory reactions in the tissue.