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The Balance of Th17 versus Treg Cells in Autoimmunity

T helper type 17 (Th17) cells and pTreg cells, which share a common precursor cell (the naïve CD4 T cell), require a common tumor growth factor (TGF)-β signal for initial differentiation. However, terminally differentiated cells fulfill opposite functions: Th17 cells cause autoimmunity and inflammat...

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Detalles Bibliográficos
Autor principal: Lee, Gap Ryol
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5877591/
https://www.ncbi.nlm.nih.gov/pubmed/29510522
http://dx.doi.org/10.3390/ijms19030730
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author Lee, Gap Ryol
author_facet Lee, Gap Ryol
author_sort Lee, Gap Ryol
collection PubMed
description T helper type 17 (Th17) cells and pTreg cells, which share a common precursor cell (the naïve CD4 T cell), require a common tumor growth factor (TGF)-β signal for initial differentiation. However, terminally differentiated cells fulfill opposite functions: Th17 cells cause autoimmunity and inflammation, whereas Treg cells inhibit these phenomena and maintain immune homeostasis. Thus, unraveling the mechanisms that affect the Th17/Treg cell balance is critical if we are to better understand autoimmunity and tolerance. Recent studies have identified many factors that influence this balance; these factors range from signaling pathways triggered by T cell receptors, costimulatory receptors, and cytokines, to various metabolic pathways and the intestinal microbiota. This review article summarizes recent advances in our understanding of the Th17/Treg balance and its implications with respect to autoimmune disease.
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spelling pubmed-58775912018-04-09 The Balance of Th17 versus Treg Cells in Autoimmunity Lee, Gap Ryol Int J Mol Sci Review T helper type 17 (Th17) cells and pTreg cells, which share a common precursor cell (the naïve CD4 T cell), require a common tumor growth factor (TGF)-β signal for initial differentiation. However, terminally differentiated cells fulfill opposite functions: Th17 cells cause autoimmunity and inflammation, whereas Treg cells inhibit these phenomena and maintain immune homeostasis. Thus, unraveling the mechanisms that affect the Th17/Treg cell balance is critical if we are to better understand autoimmunity and tolerance. Recent studies have identified many factors that influence this balance; these factors range from signaling pathways triggered by T cell receptors, costimulatory receptors, and cytokines, to various metabolic pathways and the intestinal microbiota. This review article summarizes recent advances in our understanding of the Th17/Treg balance and its implications with respect to autoimmune disease. MDPI 2018-03-03 /pmc/articles/PMC5877591/ /pubmed/29510522 http://dx.doi.org/10.3390/ijms19030730 Text en © 2018 by the author. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Lee, Gap Ryol
The Balance of Th17 versus Treg Cells in Autoimmunity
title The Balance of Th17 versus Treg Cells in Autoimmunity
title_full The Balance of Th17 versus Treg Cells in Autoimmunity
title_fullStr The Balance of Th17 versus Treg Cells in Autoimmunity
title_full_unstemmed The Balance of Th17 versus Treg Cells in Autoimmunity
title_short The Balance of Th17 versus Treg Cells in Autoimmunity
title_sort balance of th17 versus treg cells in autoimmunity
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5877591/
https://www.ncbi.nlm.nih.gov/pubmed/29510522
http://dx.doi.org/10.3390/ijms19030730
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