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Inflammation-associated genes: risks and benefits to Foxp3(+) regulatory T-cell function
Foxp3(+) regulatory T (Treg) cells prevent the development of autoimmunity and immunopathology, as well as maintaining homeostasis and tolerance to commensal microorganisms. The suppressive activity of Treg cells is their defining characteristic, generating great interest in their therapeutic potent...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley & Sons, Ltd
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4582961/ https://www.ncbi.nlm.nih.gov/pubmed/26190495 http://dx.doi.org/10.1111/imm.12507 |
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author | O’Connor, Richard A Anderton, Stephen M |
author_facet | O’Connor, Richard A Anderton, Stephen M |
author_sort | O’Connor, Richard A |
collection | PubMed |
description | Foxp3(+) regulatory T (Treg) cells prevent the development of autoimmunity and immunopathology, as well as maintaining homeostasis and tolerance to commensal microorganisms. The suppressive activity of Treg cells is their defining characteristic, generating great interest in their therapeutic potential. However, suppressive and effector functions are not entirely exclusive. Considerable evidence points to the ability of supposedly anti-inflammatory Foxp3-expressing Treg cells to also express transcription factors that have been characterized as cardinal drivers of T effector cell function. We will consider the mounting evidence that Treg cells can function in non-suppressive capacities and review the impetus for this functional change, its relevance to developing immune and autoimmune responses and its significance to the development of Treg-based therapies. |
format | Online Article Text |
id | pubmed-4582961 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | John Wiley & Sons, Ltd |
record_format | MEDLINE/PubMed |
spelling | pubmed-45829612016-10-01 Inflammation-associated genes: risks and benefits to Foxp3(+) regulatory T-cell function O’Connor, Richard A Anderton, Stephen M Immunology Review Articles Foxp3(+) regulatory T (Treg) cells prevent the development of autoimmunity and immunopathology, as well as maintaining homeostasis and tolerance to commensal microorganisms. The suppressive activity of Treg cells is their defining characteristic, generating great interest in their therapeutic potential. However, suppressive and effector functions are not entirely exclusive. Considerable evidence points to the ability of supposedly anti-inflammatory Foxp3-expressing Treg cells to also express transcription factors that have been characterized as cardinal drivers of T effector cell function. We will consider the mounting evidence that Treg cells can function in non-suppressive capacities and review the impetus for this functional change, its relevance to developing immune and autoimmune responses and its significance to the development of Treg-based therapies. John Wiley & Sons, Ltd 2015-10 2015-09-09 /pmc/articles/PMC4582961/ /pubmed/26190495 http://dx.doi.org/10.1111/imm.12507 Text en © 2015 John Wiley & Sons Ltd |
spellingShingle | Review Articles O’Connor, Richard A Anderton, Stephen M Inflammation-associated genes: risks and benefits to Foxp3(+) regulatory T-cell function |
title | Inflammation-associated genes: risks and benefits to Foxp3(+) regulatory T-cell function |
title_full | Inflammation-associated genes: risks and benefits to Foxp3(+) regulatory T-cell function |
title_fullStr | Inflammation-associated genes: risks and benefits to Foxp3(+) regulatory T-cell function |
title_full_unstemmed | Inflammation-associated genes: risks and benefits to Foxp3(+) regulatory T-cell function |
title_short | Inflammation-associated genes: risks and benefits to Foxp3(+) regulatory T-cell function |
title_sort | inflammation-associated genes: risks and benefits to foxp3(+) regulatory t-cell function |
topic | Review Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4582961/ https://www.ncbi.nlm.nih.gov/pubmed/26190495 http://dx.doi.org/10.1111/imm.12507 |
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