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Аннотация
Coeliac disease (CD), also called celiac disease, celiac sprue and gluten-sensitive enteropathy, is a genetically determined, polygenic autoimmune disease with a transmission, which doesn't obey the laws of simple Mendelian inheritance.It causes acute intestinal damage and affects other body systems as a result of eating food products containing gluten.The term "gluten" includes two main groups of storage proteins found in certain cereal grains: the glutenin group and the prolamin group [1].The wheat is the most widespread gluten cereal in food production, and its prolamins are called gliadins.The Codex Alimentarius defines the glutenfree food product as the product with the gluten proteins level in it lower than 20 mg/kg in total, and people with gluten intolerance (such as coeliac disease patients) can eat this kind of foods.Currently, there is only one possible option of coeliac disease treatmentgluten-free diet.Coeliac disease is diagnosed via presence of HLA-DQ2/DQ8 haplotypes, and over 98% of people with CD carry the DQ2 or DQ8 HLA class II alleles [2].The overall incidence of these haplotypes between people without coeliac disease is over 50%, so genetic predisposition to coeliac disease is partly determined by HLA-DQ variants, and partly by single nucleotide polymorphisms (SNPs) in other genes.Molecular mechanism initiating autoimmune reaction to gluten in coeliac disease begins in the lumen of the intestine, where gluten proteins go through a partial proteolysis (Fig. 1).After that, the processed gluten oligopeptides are transported enterocytes and intraepithelial lymphocytes 3S3J 3S3S 2Q3Z Gliadin oligopeptide
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