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Th17 Cells in Type 1 Diabetes: Role in the Pathogenesis and Regulation by Gut Microbiome

Type 1 diabetes (T1D) is an autoimmune disease which is characterized by progressive destruction of insulin producing pancreatic islet β cells. The risk of developing T1D is determined by both genetic and environmental factors. A growing body of evidence supports an important role of T helper type 1...

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Detalles Bibliográficos
Autores principales: Li, Yangyang, Liu, Yu, Chu, Cong-Qiu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4710950/
https://www.ncbi.nlm.nih.gov/pubmed/26843788
http://dx.doi.org/10.1155/2015/638470
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author Li, Yangyang
Liu, Yu
Chu, Cong-Qiu
author_facet Li, Yangyang
Liu, Yu
Chu, Cong-Qiu
author_sort Li, Yangyang
collection PubMed
description Type 1 diabetes (T1D) is an autoimmune disease which is characterized by progressive destruction of insulin producing pancreatic islet β cells. The risk of developing T1D is determined by both genetic and environmental factors. A growing body of evidence supports an important role of T helper type 17 (Th17) cells along with impaired T regulatory (Treg) cells in the development of T1D in animal models and humans. Alteration of gut microbiota has been implicated to be responsible for the imbalance between Th17 and Treg cells. However, there is controversy concerning a pathogenic versus protective role of Th17 cells in murine models of diabetes in the context of influence of gut microbiota. In this review we will summarize current knowledge about Th17 cells and gut microbiota involved in T1D and propose Th17 targeted therapy in children with islet autoimmunity to prevent progression to overt diabetes.
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spelling pubmed-47109502016-02-03 Th17 Cells in Type 1 Diabetes: Role in the Pathogenesis and Regulation by Gut Microbiome Li, Yangyang Liu, Yu Chu, Cong-Qiu Mediators Inflamm Review Article Type 1 diabetes (T1D) is an autoimmune disease which is characterized by progressive destruction of insulin producing pancreatic islet β cells. The risk of developing T1D is determined by both genetic and environmental factors. A growing body of evidence supports an important role of T helper type 17 (Th17) cells along with impaired T regulatory (Treg) cells in the development of T1D in animal models and humans. Alteration of gut microbiota has been implicated to be responsible for the imbalance between Th17 and Treg cells. However, there is controversy concerning a pathogenic versus protective role of Th17 cells in murine models of diabetes in the context of influence of gut microbiota. In this review we will summarize current knowledge about Th17 cells and gut microbiota involved in T1D and propose Th17 targeted therapy in children with islet autoimmunity to prevent progression to overt diabetes. Hindawi Publishing Corporation 2015 2015-12-30 /pmc/articles/PMC4710950/ /pubmed/26843788 http://dx.doi.org/10.1155/2015/638470 Text en Copyright © 2015 Yangyang Li et al. https://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Li, Yangyang
Liu, Yu
Chu, Cong-Qiu
Th17 Cells in Type 1 Diabetes: Role in the Pathogenesis and Regulation by Gut Microbiome
title Th17 Cells in Type 1 Diabetes: Role in the Pathogenesis and Regulation by Gut Microbiome
title_full Th17 Cells in Type 1 Diabetes: Role in the Pathogenesis and Regulation by Gut Microbiome
title_fullStr Th17 Cells in Type 1 Diabetes: Role in the Pathogenesis and Regulation by Gut Microbiome
title_full_unstemmed Th17 Cells in Type 1 Diabetes: Role in the Pathogenesis and Regulation by Gut Microbiome
title_short Th17 Cells in Type 1 Diabetes: Role in the Pathogenesis and Regulation by Gut Microbiome
title_sort th17 cells in type 1 diabetes: role in the pathogenesis and regulation by gut microbiome
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4710950/
https://www.ncbi.nlm.nih.gov/pubmed/26843788
http://dx.doi.org/10.1155/2015/638470
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