Hyperosmolarity impedes the cross-priming competence of dendritic cells in a TRIF-dependent manner

Abstract Tissue osmolarity varies among different organs and can be considerably increased under pathologic conditions. Hyperosmolarity has been associated with altered stimulatory properties of immune cells, especially macrophages and dendritic cells. We have recently reported that dendritic cells...

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Autores principales:	Zoran V. Popovic, Maria Embgenbroich, Federica Chessa, Viola Nordström, Mahnaz Bonrouhi, Thomas Hielscher, Norbert Gretz, Shijun Wang, Daniel Mathow, Thomas Quast, Jan-Gero Schloetel, Waldemar Kolanus, Sven Burgdorf, Hermann-Josef Gröne
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/f4e2374515c948a5bcaeab086834c60c
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spelling	oai:doaj.org-article:f4e2374515c948a5bcaeab086834c60c2021-12-02T15:05:35ZHyperosmolarity impedes the cross-priming competence of dendritic cells in a TRIF-dependent manner10.1038/s41598-017-00434-y2045-2322https://doaj.org/article/f4e2374515c948a5bcaeab086834c60c2017-03-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-00434-yhttps://doaj.org/toc/2045-2322Abstract Tissue osmolarity varies among different organs and can be considerably increased under pathologic conditions. Hyperosmolarity has been associated with altered stimulatory properties of immune cells, especially macrophages and dendritic cells. We have recently reported that dendritic cells upon exposure to hypertonic stimuli shift their profile towards a macrophage-M2-like phenotype, resulting in attenuated local alloreactivity during acute kidney graft rejection. Here, we examined how hyperosmotic microenvironment affects the cross-priming capacity of dendritic cells. Using ovalbumin as model antigen, we showed that exposure of dendritic cells to hyperosmolarity strongly inhibits activation of antigen-specific T cells despite enhancement of antigen uptake, processing and presentation. We identified TRIF as key mediator of this phenomenon. Moreover, we detected a hyperosmolarity-triggered, TRIF-dependent clustering of MHCI loaded with the ovalbumin-derived epitope, but not of overall MHCI molecules, providing a possible explanation for a reduced T cell activation. Our findings identify dendritic cells as important players in hyperosmolarity-mediated immune imbalance and provide evidence for a novel pathway of inhibition of antigen specific CD8+ T cell response in a hypertonic micromilieu.Zoran V. PopovicMaria EmbgenbroichFederica ChessaViola NordströmMahnaz BonrouhiThomas HielscherNorbert GretzShijun WangDaniel MathowThomas QuastJan-Gero SchloetelWaldemar KolanusSven BurgdorfHermann-Josef GröneNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-14 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Zoran V. Popovic Maria Embgenbroich Federica Chessa Viola Nordström Mahnaz Bonrouhi Thomas Hielscher Norbert Gretz Shijun Wang Daniel Mathow Thomas Quast Jan-Gero Schloetel Waldemar Kolanus Sven Burgdorf Hermann-Josef Gröne Hyperosmolarity impedes the cross-priming competence of dendritic cells in a TRIF-dependent manner
description	Abstract Tissue osmolarity varies among different organs and can be considerably increased under pathologic conditions. Hyperosmolarity has been associated with altered stimulatory properties of immune cells, especially macrophages and dendritic cells. We have recently reported that dendritic cells upon exposure to hypertonic stimuli shift their profile towards a macrophage-M2-like phenotype, resulting in attenuated local alloreactivity during acute kidney graft rejection. Here, we examined how hyperosmotic microenvironment affects the cross-priming capacity of dendritic cells. Using ovalbumin as model antigen, we showed that exposure of dendritic cells to hyperosmolarity strongly inhibits activation of antigen-specific T cells despite enhancement of antigen uptake, processing and presentation. We identified TRIF as key mediator of this phenomenon. Moreover, we detected a hyperosmolarity-triggered, TRIF-dependent clustering of MHCI loaded with the ovalbumin-derived epitope, but not of overall MHCI molecules, providing a possible explanation for a reduced T cell activation. Our findings identify dendritic cells as important players in hyperosmolarity-mediated immune imbalance and provide evidence for a novel pathway of inhibition of antigen specific CD8+ T cell response in a hypertonic micromilieu.
format	article
author	Zoran V. Popovic Maria Embgenbroich Federica Chessa Viola Nordström Mahnaz Bonrouhi Thomas Hielscher Norbert Gretz Shijun Wang Daniel Mathow Thomas Quast Jan-Gero Schloetel Waldemar Kolanus Sven Burgdorf Hermann-Josef Gröne
author_facet	Zoran V. Popovic Maria Embgenbroich Federica Chessa Viola Nordström Mahnaz Bonrouhi Thomas Hielscher Norbert Gretz Shijun Wang Daniel Mathow Thomas Quast Jan-Gero Schloetel Waldemar Kolanus Sven Burgdorf Hermann-Josef Gröne
author_sort	Zoran V. Popovic
title	Hyperosmolarity impedes the cross-priming competence of dendritic cells in a TRIF-dependent manner
title_short	Hyperosmolarity impedes the cross-priming competence of dendritic cells in a TRIF-dependent manner
title_full	Hyperosmolarity impedes the cross-priming competence of dendritic cells in a TRIF-dependent manner
title_fullStr	Hyperosmolarity impedes the cross-priming competence of dendritic cells in a TRIF-dependent manner
title_full_unstemmed	Hyperosmolarity impedes the cross-priming competence of dendritic cells in a TRIF-dependent manner
title_sort	hyperosmolarity impedes the cross-priming competence of dendritic cells in a trif-dependent manner
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/f4e2374515c948a5bcaeab086834c60c
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Hyperosmolarity impedes the cross-priming competence of dendritic cells in a TRIF-dependent manner

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