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Regulation of plasmacytoid dendritic cell development in mice by aryl hydrocarbon receptor

Aryl hydrocarbon receptor (AhR) plays an important role in the regulation of cell responses to different environmental stimuli, as well as to various endogenous ligands. Although AhR was previously implicated in the regulation of dendritic cell (DC) activation, very little is known about its potenti...

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Autores principales: Liu, Hao, Ramachandran, Indu, Gabrilovich, Dmitry I.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3945671/
https://www.ncbi.nlm.nih.gov/pubmed/24165981
http://dx.doi.org/10.1038/icb.2013.65
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author Liu, Hao
Ramachandran, Indu
Gabrilovich, Dmitry I.
author_facet Liu, Hao
Ramachandran, Indu
Gabrilovich, Dmitry I.
author_sort Liu, Hao
collection PubMed
description Aryl hydrocarbon receptor (AhR) plays an important role in the regulation of cell responses to different environmental stimuli, as well as to various endogenous ligands. Although AhR was previously implicated in the regulation of dendritic cell (DC) activation, very little is known about its potential role in the development of these cells. Here, we report our unexpected findings that AhR may regulate the differentiation of plasmacytoid DCs (pDCs). Agonist of AhR dramatically decreased the generation of pDCs in vitro, while the AhR antagonist had an opposite effect. The differentiation of conventional DCs (cDCs) was not affected. AhR knockout mice had a substantial accumulation of pDCs in peripheral lymphoid organs; whereas, no changes in cDCs were seen. Thus, this study has identified AhR as a transcription factor involved in the development of one population of DCs - pDCs.
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spelling pubmed-39456712014-08-01 Regulation of plasmacytoid dendritic cell development in mice by aryl hydrocarbon receptor Liu, Hao Ramachandran, Indu Gabrilovich, Dmitry I. Immunol Cell Biol Article Aryl hydrocarbon receptor (AhR) plays an important role in the regulation of cell responses to different environmental stimuli, as well as to various endogenous ligands. Although AhR was previously implicated in the regulation of dendritic cell (DC) activation, very little is known about its potential role in the development of these cells. Here, we report our unexpected findings that AhR may regulate the differentiation of plasmacytoid DCs (pDCs). Agonist of AhR dramatically decreased the generation of pDCs in vitro, while the AhR antagonist had an opposite effect. The differentiation of conventional DCs (cDCs) was not affected. AhR knockout mice had a substantial accumulation of pDCs in peripheral lymphoid organs; whereas, no changes in cDCs were seen. Thus, this study has identified AhR as a transcription factor involved in the development of one population of DCs - pDCs. 2013-10-29 2014-02 /pmc/articles/PMC3945671/ /pubmed/24165981 http://dx.doi.org/10.1038/icb.2013.65 Text en Users may view, print, copy, download and text and data- mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use: http://www.nature.com/authors/editorial_policies/license.html#terms
spellingShingle Article
Liu, Hao
Ramachandran, Indu
Gabrilovich, Dmitry I.
Regulation of plasmacytoid dendritic cell development in mice by aryl hydrocarbon receptor
title Regulation of plasmacytoid dendritic cell development in mice by aryl hydrocarbon receptor
title_full Regulation of plasmacytoid dendritic cell development in mice by aryl hydrocarbon receptor
title_fullStr Regulation of plasmacytoid dendritic cell development in mice by aryl hydrocarbon receptor
title_full_unstemmed Regulation of plasmacytoid dendritic cell development in mice by aryl hydrocarbon receptor
title_short Regulation of plasmacytoid dendritic cell development in mice by aryl hydrocarbon receptor
title_sort regulation of plasmacytoid dendritic cell development in mice by aryl hydrocarbon receptor
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3945671/
https://www.ncbi.nlm.nih.gov/pubmed/24165981
http://dx.doi.org/10.1038/icb.2013.65
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