Coeliac disease (CD) is an autoimmune disorder of the small intestine that results from the immune response to various cereal proteins, mostly gliadin. It is a genetically determined disease; among predisposing genes those of the HLA complex are of paramount importance, especially the alleles coding for HLA-DQ2 (90-95 % of CD patients) and HLA–DQ8 (3 - 5 % of CD patients) molecules, respectively. They present a peptide originating from gliadin to autoreactive T-cell. However, before they are able to do it, gliadin has to be deaminated by a tissue transglutaminase 2. TH1- cell mediated immune response is responsible for immunopathological changes, which are very efficiently supported by IgA anti - TG2 autoantibodies. The formed immunocomplexes are deposited into subepithelial layer of the intestine. As polymeric forms of IgA are able to activate the lectine pathway of the complement system, is it activated and contributes to inflammatory processes. Some patients also produce autoantibodies against epidermal transglataminase what can result into the development of dermatitis herpertiformis.