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Molecular mechanisms underlying Th1-like Treg generation and function

Since their ‘re-discovery’ more than two decades ago, FOXP3(+) regulatory T cells (Tregs) have been an important subject of investigation in the biomedical field and our understanding of the mechanisms that drive their phenotype and function in health and disease has advanced tremendously. During th...

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Detalles Bibliográficos
Autores principales: Kitz, Alexandra, Dominguez-Villar, Margarita
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer International Publishing 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7079789/
https://www.ncbi.nlm.nih.gov/pubmed/28624966
http://dx.doi.org/10.1007/s00018-017-2569-y
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author Kitz, Alexandra
Dominguez-Villar, Margarita
author_facet Kitz, Alexandra
Dominguez-Villar, Margarita
author_sort Kitz, Alexandra
collection PubMed
description Since their ‘re-discovery’ more than two decades ago, FOXP3(+) regulatory T cells (Tregs) have been an important subject of investigation in the biomedical field and our understanding of the mechanisms that drive their phenotype and function in health and disease has advanced tremendously. During the past few years it has become clear that Tregs are not a terminally differentiated population but show some degree of plasticity, and can, under specific environmental conditions, acquire the phenotype of effector T cells. In particular, recent works have highlighted the acquisition of a Th1-like phenotype by Tregs in several pathological environments. In this review we give an update on the concept of Treg plasticity and the advances in defining the molecular mechanisms that underlie the generation of Th1-like Tregs during an immune response and in different disease settings.
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spelling pubmed-70797892020-03-23 Molecular mechanisms underlying Th1-like Treg generation and function Kitz, Alexandra Dominguez-Villar, Margarita Cell Mol Life Sci Review Since their ‘re-discovery’ more than two decades ago, FOXP3(+) regulatory T cells (Tregs) have been an important subject of investigation in the biomedical field and our understanding of the mechanisms that drive their phenotype and function in health and disease has advanced tremendously. During the past few years it has become clear that Tregs are not a terminally differentiated population but show some degree of plasticity, and can, under specific environmental conditions, acquire the phenotype of effector T cells. In particular, recent works have highlighted the acquisition of a Th1-like phenotype by Tregs in several pathological environments. In this review we give an update on the concept of Treg plasticity and the advances in defining the molecular mechanisms that underlie the generation of Th1-like Tregs during an immune response and in different disease settings. Springer International Publishing 2017-06-17 2017 /pmc/articles/PMC7079789/ /pubmed/28624966 http://dx.doi.org/10.1007/s00018-017-2569-y Text en © Springer International Publishing AG 2017 This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic.
spellingShingle Review
Kitz, Alexandra
Dominguez-Villar, Margarita
Molecular mechanisms underlying Th1-like Treg generation and function
title Molecular mechanisms underlying Th1-like Treg generation and function
title_full Molecular mechanisms underlying Th1-like Treg generation and function
title_fullStr Molecular mechanisms underlying Th1-like Treg generation and function
title_full_unstemmed Molecular mechanisms underlying Th1-like Treg generation and function
title_short Molecular mechanisms underlying Th1-like Treg generation and function
title_sort molecular mechanisms underlying th1-like treg generation and function
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7079789/
https://www.ncbi.nlm.nih.gov/pubmed/28624966
http://dx.doi.org/10.1007/s00018-017-2569-y
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