Abstract
Celiac Disease (CD) is an immune-mediated systemic disorder elicited by gluten and related prolamines in genetically susceptible individuals and it is the result of the interaction between genetic and environmental factors. Among genetic risk factors, the strongest association is with the HLA class II DQ region; nevertheless at least 39 non-HLA loci are associated with CD. Gluten is the main environmental trigger of the disease. In addition, infant feeding and weaning practices as well as timing of gluten introduction in the diet have been suggested to contribute to CD risk. Furthermore a role for infectious agents and microbiota composition in disease development has also been proposed.Aim of this short review is to discuss the current knowledge on both genetic and environmental risk factors for the development of CD; moreover we will provide a brief overview of the possible strategies that could be envisaged to prevent this condition, at least in the population at-risk.
Highlights
Celiac Disease (CD) is an immune-mediated systemic disorder elicited by gluten and related prolamines in genetically susceptible individuals, carrying the human leukocyte antigen (HLA)-DQ2 or HLA-DQ8 haplotypes, and characterized by the presence of a variable combination of gluten-dependent clinical manifestations, CDspecific antibodies, and a small intestinal enteropathy [1]
Among genetic factors associated with CD, the strongest association is with the HLA class II region
The results showed a cumulative incidence of CD at 3 years of age similar in the gluten group and placebo group (5,9 % and 4,5 % respectively)
Summary
Celiac Disease (CD) is an immune-mediated systemic disorder elicited by gluten and related prolamines in genetically susceptible individuals, carrying the human leukocyte antigen (HLA)-DQ2 or HLA-DQ8 haplotypes, and characterized by the presence of a variable combination of gluten-dependent clinical manifestations, CDspecific antibodies, and a small intestinal enteropathy [1]. Gluten peptides, modified by tissue transglutaminase, are able to elicit both an innate and an adaptive HLA-restricted gluten specific immune response in the intestinal mucosa of genetically predisposed subjects, resulting in the infiltration of the epithelium with lymphocytes and tissue remodeling leading to villous atrophy [2]. Aim of this short review is to discuss the current knowledge on genetic and environmental risk factors involved in CD pathogenesis, and the possible strategies that could be envisaged to prevent disease development, at least in at-risk subjects
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