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Th17, intestinal microbiota and the abnormal immune response in the pathogenesis of celiac disease

Celiac disease (CD) is an autoimmune enteropathy induced by the ingestion of gluten in genetically predisposed individuals who carry the HLA-DQ2 or -DQ8 alleles. The immune response is abnormal in celiac disease with small intestinal epithelial damage via CD8+CD4- intraepithelial lymphocytes. The et...

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Autores principales: Cicerone, Clelia, Nenna, Raffaella, Pontone, Stefano
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Shaheed Beheshti University of Medical Sciences 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4404588/
https://www.ncbi.nlm.nih.gov/pubmed/25926936
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author Cicerone, Clelia
Nenna, Raffaella
Pontone, Stefano
author_facet Cicerone, Clelia
Nenna, Raffaella
Pontone, Stefano
author_sort Cicerone, Clelia
collection PubMed
description Celiac disease (CD) is an autoimmune enteropathy induced by the ingestion of gluten in genetically predisposed individuals who carry the HLA-DQ2 or -DQ8 alleles. The immune response is abnormal in celiac disease with small intestinal epithelial damage via CD8+CD4- intraepithelial lymphocytes. The etiology is multifactorial involving genetic and environmental factors, an abnormal immune response, and intestinal dysbiosis. The innate and acquired T-cell mediated immunity play important roles in the pathogenesis of this disease, particularly CD4+ Th17 cells, which have been shown to have critical functions in host defense against bacterial pathogens and in the inflammatory responses to deamidated gluten peptides. We review what is known about the interaction between immune system and intestinal microbiota in the pathogenesis of celiac disease.
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spelling pubmed-44045882015-04-29 Th17, intestinal microbiota and the abnormal immune response in the pathogenesis of celiac disease Cicerone, Clelia Nenna, Raffaella Pontone, Stefano Gastroenterol Hepatol Bed Bench Review Article Celiac disease (CD) is an autoimmune enteropathy induced by the ingestion of gluten in genetically predisposed individuals who carry the HLA-DQ2 or -DQ8 alleles. The immune response is abnormal in celiac disease with small intestinal epithelial damage via CD8+CD4- intraepithelial lymphocytes. The etiology is multifactorial involving genetic and environmental factors, an abnormal immune response, and intestinal dysbiosis. The innate and acquired T-cell mediated immunity play important roles in the pathogenesis of this disease, particularly CD4+ Th17 cells, which have been shown to have critical functions in host defense against bacterial pathogens and in the inflammatory responses to deamidated gluten peptides. We review what is known about the interaction between immune system and intestinal microbiota in the pathogenesis of celiac disease. Shaheed Beheshti University of Medical Sciences 2015 /pmc/articles/PMC4404588/ /pubmed/25926936 Text en This is an Open Access article distributed under the terms of the Creative Commons Attribution License, (http://creativecommons.org/licenses/by/3.0/) which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Cicerone, Clelia
Nenna, Raffaella
Pontone, Stefano
Th17, intestinal microbiota and the abnormal immune response in the pathogenesis of celiac disease
title Th17, intestinal microbiota and the abnormal immune response in the pathogenesis of celiac disease
title_full Th17, intestinal microbiota and the abnormal immune response in the pathogenesis of celiac disease
title_fullStr Th17, intestinal microbiota and the abnormal immune response in the pathogenesis of celiac disease
title_full_unstemmed Th17, intestinal microbiota and the abnormal immune response in the pathogenesis of celiac disease
title_short Th17, intestinal microbiota and the abnormal immune response in the pathogenesis of celiac disease
title_sort th17, intestinal microbiota and the abnormal immune response in the pathogenesis of celiac disease
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4404588/
https://www.ncbi.nlm.nih.gov/pubmed/25926936
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