The Treg/Th17 Axis: A Dynamic Balance Regulated by the Gut Microbiome

T-helper 17 (Th17) and T-regulatory (Treg) cells are frequently found at barrier surfaces, particularly within the intestinal mucosa, where they function to protect the host from pathogenic microorganisms and to restrain excessive effector T-cell responses, respectively. Despite their differing func...

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Main Authors:	Omenetti, Sara, Pizarro, Theresa T.
Format:	Online
Language:	English
Published:	Frontiers Media S.A. 2015
Online Access:	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4681807/

id	pubmed-4681807
recordtype	oai_dc
spelling	pubmed-46818072016-01-05 The Treg/Th17 Axis: A Dynamic Balance Regulated by the Gut Microbiome Omenetti, Sara Pizarro, Theresa T. Immunology T-helper 17 (Th17) and T-regulatory (Treg) cells are frequently found at barrier surfaces, particularly within the intestinal mucosa, where they function to protect the host from pathogenic microorganisms and to restrain excessive effector T-cell responses, respectively. Despite their differing functional properties, Th17 cells and Tregs share similar developmental requirements. In fact, the fate of antigen-naïve T-cells to either Th17 or Treg lineages is finely regulated by key mediators, including TGFβ, IL-6, and all-trans retinoic acid. Importantly, the intestinal microbiome also provides immunostimulatory signals, which can activate innate and downstream adaptive immune responses. Specific components of the gut microbiome have been implicated in the production of proinflammatory cytokines by innate immune cells, such as IL-6, IL-23, IL-1β, and the subsequent generation and expansion of Th17 cells. Similarly, commensal bacteria and their metabolites can also promote the generation of intestinal Tregs that can actively induce mucosal tolerance. As such, dysbiosis of the gut microbiome may not solely represent a consequence of gut inflammation, but rather shape the Treg/Th17 commitment and influence susceptibility to inflammatory bowel disease. In this review, we discuss Treg and Th17 cell plasticity, its dynamic regulation by the microbiome, and highlight its impact on intestinal homeostasis and disease. Frontiers Media S.A. 2015-12-17 /pmc/articles/PMC4681807/ /pubmed/26734006 http://dx.doi.org/10.3389/fimmu.2015.00639 Text en Copyright © 2015 Omenetti and Pizarro. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
repository_type	Open Access Journal
institution_category	Foreign Institution
institution	US National Center for Biotechnology Information
building	NCBI PubMed
collection	Online Access
language	English
format	Online
author	Omenetti, Sara Pizarro, Theresa T.
spellingShingle	Omenetti, Sara Pizarro, Theresa T. The Treg/Th17 Axis: A Dynamic Balance Regulated by the Gut Microbiome
author_facet	Omenetti, Sara Pizarro, Theresa T.
author_sort	Omenetti, Sara
title	The Treg/Th17 Axis: A Dynamic Balance Regulated by the Gut Microbiome
title_short	The Treg/Th17 Axis: A Dynamic Balance Regulated by the Gut Microbiome
title_full	The Treg/Th17 Axis: A Dynamic Balance Regulated by the Gut Microbiome
title_fullStr	The Treg/Th17 Axis: A Dynamic Balance Regulated by the Gut Microbiome
title_full_unstemmed	The Treg/Th17 Axis: A Dynamic Balance Regulated by the Gut Microbiome
title_sort	treg/th17 axis: a dynamic balance regulated by the gut microbiome
description	T-helper 17 (Th17) and T-regulatory (Treg) cells are frequently found at barrier surfaces, particularly within the intestinal mucosa, where they function to protect the host from pathogenic microorganisms and to restrain excessive effector T-cell responses, respectively. Despite their differing functional properties, Th17 cells and Tregs share similar developmental requirements. In fact, the fate of antigen-naïve T-cells to either Th17 or Treg lineages is finely regulated by key mediators, including TGFβ, IL-6, and all-trans retinoic acid. Importantly, the intestinal microbiome also provides immunostimulatory signals, which can activate innate and downstream adaptive immune responses. Specific components of the gut microbiome have been implicated in the production of proinflammatory cytokines by innate immune cells, such as IL-6, IL-23, IL-1β, and the subsequent generation and expansion of Th17 cells. Similarly, commensal bacteria and their metabolites can also promote the generation of intestinal Tregs that can actively induce mucosal tolerance. As such, dysbiosis of the gut microbiome may not solely represent a consequence of gut inflammation, but rather shape the Treg/Th17 commitment and influence susceptibility to inflammatory bowel disease. In this review, we discuss Treg and Th17 cell plasticity, its dynamic regulation by the microbiome, and highlight its impact on intestinal homeostasis and disease.
publisher	Frontiers Media S.A.
publishDate	2015
url	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4681807/
_version_	1613513540250894336

The Treg/Th17 Axis: A Dynamic Balance Regulated by the Gut Microbiome

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