Current allergy and asthma reports · 2019
Genetic and Environmental Contributors for Celiac Disease.
СтатьяОбзорНазвание и аннотация: Перевод пока не подготовлен
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Serena Gloria, Lima Rosiane, Fasano Alessio
Аннотация
PURPOSE OF REVIEW: Celiac disease (CD) is an autoimmune enteropathy triggered by gluten. The purpose of this review is to examine the major genetic and environmental factors that contribute to CD pathogenesis.
RECENT FINDINGS: We reviewed the current state of knowledge on the genetic and environmental components that play a role in CD onset. A genome-wide association study (GWAS) analysis has highlighted several genes other than HLA involved in CD. Recent studies have shown that HLA haplotype influences the microbiome composition in infants and that dysbiosis in the intestinal microflora, in turn, contributes to loss of tolerance to gluten. Recently, observational studies have discussed the hypothesis stating that breast-feeding had a protective role against CD onset. CD etiology is influenced by genetic and environmental factors. A better understanding of these components would deepen our knowledge on the mechanisms that lead to loss of tolerance and could help in developing a more "personalized medicine."
RECENT FINDINGS: We reviewed the current state of knowledge on the genetic and environmental components that play a role in CD onset. A genome-wide association study (GWAS) analysis has highlighted several genes other than HLA involved in CD. Recent studies have shown that HLA haplotype influences the microbiome composition in infants and that dysbiosis in the intestinal microflora, in turn, contributes to loss of tolerance to gluten. Recently, observational studies have discussed the hypothesis stating that breast-feeding had a protective role against CD onset. CD etiology is influenced by genetic and environmental factors. A better understanding of these components would deepen our knowledge on the mechanisms that lead to loss of tolerance and could help in developing a more "personalized medicine."