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The Function and Role of the Th17/Treg Cell Balance in Inflammatory Bowel Disease

Inflammatory bowel disease (IBD) is a chronic, inflammatory, and autoimmune disorder. The pathogenesis of IBD is not yet clear. Studies have shown that the imbalance between T helper 17 (Th17) and regulatory T (Treg) cells, which differentiate from CD4(+) T cells, contributes to IBD. Th17 cells prom...

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Detalles Bibliográficos
Autores principales: Yan, Jun-bin, Luo, Min-min, Chen, Zhi-yun, He, Bei-hui
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7755495/
https://www.ncbi.nlm.nih.gov/pubmed/33381606
http://dx.doi.org/10.1155/2020/8813558
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author Yan, Jun-bin
Luo, Min-min
Chen, Zhi-yun
He, Bei-hui
author_facet Yan, Jun-bin
Luo, Min-min
Chen, Zhi-yun
He, Bei-hui
author_sort Yan, Jun-bin
collection PubMed
description Inflammatory bowel disease (IBD) is a chronic, inflammatory, and autoimmune disorder. The pathogenesis of IBD is not yet clear. Studies have shown that the imbalance between T helper 17 (Th17) and regulatory T (Treg) cells, which differentiate from CD4(+) T cells, contributes to IBD. Th17 cells promote tissue inflammation, and Treg cells suppress autoimmunity in IBD. Therefore, Th17/Treg cell balance is crucial. Some regulatory factors affecting the production and maintenance of these cells are also important for the proper regulation of the Th17/Treg balance; these factors include T cell receptor (TCR) signaling, costimulatory signals, cytokine signaling, bile acid metabolites, and the intestinal microbiota. This article focuses on our understanding of the function and role of the balance between Th17/Treg cells in IBD and these regulatory factors and their clinical significance in IBD.
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spelling pubmed-77554952020-12-29 The Function and Role of the Th17/Treg Cell Balance in Inflammatory Bowel Disease Yan, Jun-bin Luo, Min-min Chen, Zhi-yun He, Bei-hui J Immunol Res Review Article Inflammatory bowel disease (IBD) is a chronic, inflammatory, and autoimmune disorder. The pathogenesis of IBD is not yet clear. Studies have shown that the imbalance between T helper 17 (Th17) and regulatory T (Treg) cells, which differentiate from CD4(+) T cells, contributes to IBD. Th17 cells promote tissue inflammation, and Treg cells suppress autoimmunity in IBD. Therefore, Th17/Treg cell balance is crucial. Some regulatory factors affecting the production and maintenance of these cells are also important for the proper regulation of the Th17/Treg balance; these factors include T cell receptor (TCR) signaling, costimulatory signals, cytokine signaling, bile acid metabolites, and the intestinal microbiota. This article focuses on our understanding of the function and role of the balance between Th17/Treg cells in IBD and these regulatory factors and their clinical significance in IBD. Hindawi 2020-12-15 /pmc/articles/PMC7755495/ /pubmed/33381606 http://dx.doi.org/10.1155/2020/8813558 Text en Copyright © 2020 Jun-bin Yan 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
Yan, Jun-bin
Luo, Min-min
Chen, Zhi-yun
He, Bei-hui
The Function and Role of the Th17/Treg Cell Balance in Inflammatory Bowel Disease
title The Function and Role of the Th17/Treg Cell Balance in Inflammatory Bowel Disease
title_full The Function and Role of the Th17/Treg Cell Balance in Inflammatory Bowel Disease
title_fullStr The Function and Role of the Th17/Treg Cell Balance in Inflammatory Bowel Disease
title_full_unstemmed The Function and Role of the Th17/Treg Cell Balance in Inflammatory Bowel Disease
title_short The Function and Role of the Th17/Treg Cell Balance in Inflammatory Bowel Disease
title_sort function and role of the th17/treg cell balance in inflammatory bowel disease
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7755495/
https://www.ncbi.nlm.nih.gov/pubmed/33381606
http://dx.doi.org/10.1155/2020/8813558
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