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lüll Celiac disease: how complicated can it get?Tjon JM; van Bergen J; Koning FImmunogenetics 2010[Oct]; 62 (10): 641-51In the small intestine of celiac disease patients, dietary wheat gluten and similar proteins in barley and rye trigger an inflammatory response. While strict adherence to a gluten-free diet induces full recovery in most patients, a small percentage of patients fail to recover. In a subset of these refractory celiac disease patients, an (aberrant) oligoclonal intraepithelial lymphocyte population develops into overt lymphoma. Celiac disease is strongly associated with HLA-DQ2 and/or HLA-DQ8, as both genotypes predispose for disease development. This association can be explained by the fact that gluten peptides can be presented in HLA-DQ2 and HLA-DQ8 molecules on antigen presenting cells. Gluten-specific CD4(+) T cells in the lamina propria respond to these peptides, and this likely enhances cytotoxicity of intraepithelial lymphocytes against the intestinal epithelium. We propose a threshold model for the development of celiac disease, in which the efficiency of gluten presentation to CD4(+) T cells determines the likelihood of developing celiac disease and its complications. Key factors that influence the efficiency of gluten presentation include: (1) the level of gluten intake, (2) the enzyme tissue transglutaminase 2 which modifies gluten into high affinity binding peptides for HLA-DQ2 and HLA-DQ8, (3) the HLA-DQ type, as HLA-DQ2 binds a wider range of gluten peptides than HLA-DQ8, (4) the gene dose of HLA-DQ2 and HLA-DQ8, and finally,(5) additional genetic polymorphisms that may influence T cell reactivity. This threshold model might also help to understand the development of refractory celiac disease and lymphoma.|Adult[MESH]|Antigen Presentation[MESH]|CD4-Positive T-Lymphocytes/immunology[MESH]|Celiac Disease/epidemiology/genetics/*immunology[MESH]|Child[MESH]|Child, Preschool[MESH]|Cytotoxicity, Immunologic[MESH]|Disease Progression[MESH]|GTP-Binding Proteins[MESH]|Gene Dosage[MESH]|Genetic Association Studies[MESH]|Genetic Predisposition to Disease[MESH]|Genotype[MESH]|Glutens/immunology[MESH]|HLA-DQ Antigens/genetics/immunology[MESH]|Humans[MESH]|Immunity, Mucosal[MESH]|Intestine, Small/immunology/pathology[MESH]|Lymphoma, B-Cell, Marginal Zone/etiology[MESH]|Models, Immunological[MESH]|Prevalence[MESH]|Protein Glutamine gamma Glutamyltransferase 2[MESH]|Transglutaminases/physiology[MESH] |