Celiac disease affects 1% of the population and therefore is the most common chronic inflammation of the small intestine triggered by cereal gluten/gliadin uptake in genetically susceptible individuals. The gluten induced autoimmune disorder is characterized by autoantibodies to tissue transglutaminase (TG2), antibodies to deamidated gliadin and villous atrophy in the final stage.
TG2 plays a central role in celiac disease. Besides being the major autoantigen it is involved in the pathogenesis. Under certain circumstances and in distinct environments as given in the inflamed gut TG2 catalyzes deamidation of glutamine side chains in gliadin yielding glutamic acid. Deamidated gliadin is subsequently recognized by receptors of the immune system triggering celiac disease.
Related gluten induced autoimmune disorders are dermatitis herpetiformis / Morbus Duhring (autoantigen: epidermal transglutaminase, TG3) and neurological disorders like gluten ataxia (autoantigen: neuronal transglutaminase, TG6).