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Regulation of FoxP3(+) Regulatory T Cells and Th17 Cells by Retinoids

Vitamin A has both positive and negative regulatory functions in the immune system. While vitamin A is required for normal formation of immune cells and epithelial cell barriers, vitamin A deficiency can lead to increased inflammatory responses and tissue damage. The mechanism with which vitamin A a...

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Detalles Bibliográficos
Autor principal: Kim, Chang H.
Formato: Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2008
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2278288/
https://www.ncbi.nlm.nih.gov/pubmed/18389070
http://dx.doi.org/10.1155/2008/416910
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author Kim, Chang H.
author_facet Kim, Chang H.
author_sort Kim, Chang H.
collection PubMed
description Vitamin A has both positive and negative regulatory functions in the immune system. While vitamin A is required for normal formation of immune cells and epithelial cell barriers, vitamin A deficiency can lead to increased inflammatory responses and tissue damage. The mechanism with which vitamin A and its metabolites such as retinoids negatively regulate inflammatory responses has not been clearly defined. Recently, it has been established that retinoids promote the generation of immune-suppressive FoxP3(+) regulatory T cells while they suppress the T cell differentiation into inflammatory Th17 cells in the periphery such as intestine. These novel functions of retinoids provide a potentially important immune regulatory mechanism. In this review, we discuss the functions of retinoids in the development of the FoxP3(+) cells and Th17 cells, the phenotype and functions of retinoid-induced FoxP3(+) T cells, and the impact of retinoid-induced FoxP3(+) T cells on the immune tolerance.
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spelling pubmed-22782882008-04-03 Regulation of FoxP3(+) Regulatory T Cells and Th17 Cells by Retinoids Kim, Chang H. Clin Dev Immunol Review Article Vitamin A has both positive and negative regulatory functions in the immune system. While vitamin A is required for normal formation of immune cells and epithelial cell barriers, vitamin A deficiency can lead to increased inflammatory responses and tissue damage. The mechanism with which vitamin A and its metabolites such as retinoids negatively regulate inflammatory responses has not been clearly defined. Recently, it has been established that retinoids promote the generation of immune-suppressive FoxP3(+) regulatory T cells while they suppress the T cell differentiation into inflammatory Th17 cells in the periphery such as intestine. These novel functions of retinoids provide a potentially important immune regulatory mechanism. In this review, we discuss the functions of retinoids in the development of the FoxP3(+) cells and Th17 cells, the phenotype and functions of retinoid-induced FoxP3(+) T cells, and the impact of retinoid-induced FoxP3(+) T cells on the immune tolerance. Hindawi Publishing Corporation 2008 2008-03-19 /pmc/articles/PMC2278288/ /pubmed/18389070 http://dx.doi.org/10.1155/2008/416910 Text en Copyright © 2008 Chang H. Kim. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Kim, Chang H.
Regulation of FoxP3(+) Regulatory T Cells and Th17 Cells by Retinoids
title Regulation of FoxP3(+) Regulatory T Cells and Th17 Cells by Retinoids
title_full Regulation of FoxP3(+) Regulatory T Cells and Th17 Cells by Retinoids
title_fullStr Regulation of FoxP3(+) Regulatory T Cells and Th17 Cells by Retinoids
title_full_unstemmed Regulation of FoxP3(+) Regulatory T Cells and Th17 Cells by Retinoids
title_short Regulation of FoxP3(+) Regulatory T Cells and Th17 Cells by Retinoids
title_sort regulation of foxp3(+) regulatory t cells and th17 cells by retinoids
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2278288/
https://www.ncbi.nlm.nih.gov/pubmed/18389070
http://dx.doi.org/10.1155/2008/416910
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