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IL-17A-Producing Foxp3(+) Regulatory T Cells and Human Diseases

CD4(+)Foxp3(+) regulatory T (Treg) cells play major roles in immune homeostasis. While CD4(+)Foxp3(+) Treg cells act to suppress other immune effector cells, there is growing evidence that they also produce pro-inflammatory cytokines, such as IL-17A, in inflammatory conditions. The pro-inflammatory...

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Autores principales: Jung, Min Kyung, Kwak, Jeong-Eun, Shin, Eui-Cheol
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Korean Association of Immunologists 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5662777/
https://www.ncbi.nlm.nih.gov/pubmed/29093649
http://dx.doi.org/10.4110/in.2017.17.5.276
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author Jung, Min Kyung
Kwak, Jeong-Eun
Shin, Eui-Cheol
author_facet Jung, Min Kyung
Kwak, Jeong-Eun
Shin, Eui-Cheol
author_sort Jung, Min Kyung
collection PubMed
description CD4(+)Foxp3(+) regulatory T (Treg) cells play major roles in immune homeostasis. While CD4(+)Foxp3(+) Treg cells act to suppress other immune effector cells, there is growing evidence that they also produce pro-inflammatory cytokines, such as IL-17A, in inflammatory conditions. The pro-inflammatory cytokine milieu, toll-like receptor (TLR) signaling, and specific transcription factors are important for the production of IL-17A by CD4(+)Foxp3(+) Treg cells. In particular, IL-17A-producing CD4(+)Foxp3(+) Treg cells express RORγt, the T helper (Th) 17-specific transcription factor, in addition to Foxp3. IL-17A-producing CD4(+)Foxp3(+) Treg cells are also involved in the pathogenesis of various diseases. Here we review the mechanisms underlying the induction of IL-17A-producing CD4(+)Foxp3(+) Treg cells and the roles of these cells in human disease.
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spelling pubmed-56627772017-11-01 IL-17A-Producing Foxp3(+) Regulatory T Cells and Human Diseases Jung, Min Kyung Kwak, Jeong-Eun Shin, Eui-Cheol Immune Netw Review Article CD4(+)Foxp3(+) regulatory T (Treg) cells play major roles in immune homeostasis. While CD4(+)Foxp3(+) Treg cells act to suppress other immune effector cells, there is growing evidence that they also produce pro-inflammatory cytokines, such as IL-17A, in inflammatory conditions. The pro-inflammatory cytokine milieu, toll-like receptor (TLR) signaling, and specific transcription factors are important for the production of IL-17A by CD4(+)Foxp3(+) Treg cells. In particular, IL-17A-producing CD4(+)Foxp3(+) Treg cells express RORγt, the T helper (Th) 17-specific transcription factor, in addition to Foxp3. IL-17A-producing CD4(+)Foxp3(+) Treg cells are also involved in the pathogenesis of various diseases. Here we review the mechanisms underlying the induction of IL-17A-producing CD4(+)Foxp3(+) Treg cells and the roles of these cells in human disease. The Korean Association of Immunologists 2017-10 2017-10-16 /pmc/articles/PMC5662777/ /pubmed/29093649 http://dx.doi.org/10.4110/in.2017.17.5.276 Text en Copyright © 2017. The Korean Association of Immunologists https://creativecommons.org/licenses/by-nc/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (https://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Jung, Min Kyung
Kwak, Jeong-Eun
Shin, Eui-Cheol
IL-17A-Producing Foxp3(+) Regulatory T Cells and Human Diseases
title IL-17A-Producing Foxp3(+) Regulatory T Cells and Human Diseases
title_full IL-17A-Producing Foxp3(+) Regulatory T Cells and Human Diseases
title_fullStr IL-17A-Producing Foxp3(+) Regulatory T Cells and Human Diseases
title_full_unstemmed IL-17A-Producing Foxp3(+) Regulatory T Cells and Human Diseases
title_short IL-17A-Producing Foxp3(+) Regulatory T Cells and Human Diseases
title_sort il-17a-producing foxp3(+) regulatory t cells and human diseases
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5662777/
https://www.ncbi.nlm.nih.gov/pubmed/29093649
http://dx.doi.org/10.4110/in.2017.17.5.276
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