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DNAM-1 and PVR Regulate Monocyte Migration through Endothelial Junctions

DNAX accessory molecule 1 (DNAM-1; CD226) is a transmembrane glycoprotein involved in T cell and natural killer (NK) cell cytotoxicity. We demonstrated recently that DNAM-1 triggers NK cell–mediated killing of tumor cells upon engagement by its two ligands, poliovirus receptor (PVR; CD155) and Necti...

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Autores principales: Reymond, Nicolas, Imbert, Anne-Marie, Devilard, Elisabeth, Fabre, Stéphanie, Chabannon, Christian, Xerri, Luc, Farnarier, Catherine, Cantoni, Claudia, Bottino, Cristina, Moretta, Alessandro, Dubreuil, Patrice, Lopez, Marc
Formato: Texto
Lenguaje:English
Publicado: The Rockefeller University Press 2004
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2211807/
https://www.ncbi.nlm.nih.gov/pubmed/15136589
http://dx.doi.org/10.1084/jem.20032206
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author Reymond, Nicolas
Imbert, Anne-Marie
Devilard, Elisabeth
Fabre, Stéphanie
Chabannon, Christian
Xerri, Luc
Farnarier, Catherine
Cantoni, Claudia
Bottino, Cristina
Moretta, Alessandro
Dubreuil, Patrice
Lopez, Marc
author_facet Reymond, Nicolas
Imbert, Anne-Marie
Devilard, Elisabeth
Fabre, Stéphanie
Chabannon, Christian
Xerri, Luc
Farnarier, Catherine
Cantoni, Claudia
Bottino, Cristina
Moretta, Alessandro
Dubreuil, Patrice
Lopez, Marc
author_sort Reymond, Nicolas
collection PubMed
description DNAX accessory molecule 1 (DNAM-1; CD226) is a transmembrane glycoprotein involved in T cell and natural killer (NK) cell cytotoxicity. We demonstrated recently that DNAM-1 triggers NK cell–mediated killing of tumor cells upon engagement by its two ligands, poliovirus receptor (PVR; CD155) and Nectin-2 (CD112). In the present paper, we show that PVR and Nectin-2 are expressed at cell junctions on primary vascular endothelial cells. Moreover, the specific binding of a soluble DNAM-1–Fc molecule was detected at endothelial junctions. This binding was almost completely abrogated by anti-PVR monoclonal antibodies (mAbs), but not modified by anti–Nectin-2 mAbs, which demonstrates that PVR is the major DNAM-1 ligand on endothelial cells. Because DNAM-1 is highly expressed on leukocytes, we investigated the role of the DNAM-1–PVR interaction during the monocyte transendothelial migration process. In vitro, both anti–DNAM-1 and anti-PVR mAbs strongly blocked the transmigration of monocytes through the endothelium. Moreover, after anti–DNAM-1 or anti-PVR mAb treatment, monocytes were arrested at the apical surface of the endothelium over intercellular junctions, which strongly suggests that the DNAM-1–PVR interaction occurs during the diapedesis step. Altogether, our results demonstrate that DNAM-1 regulates monocyte extravasation via its interaction with PVR expressed at endothelial junctions on normal cells.
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spelling pubmed-22118072008-03-11 DNAM-1 and PVR Regulate Monocyte Migration through Endothelial Junctions Reymond, Nicolas Imbert, Anne-Marie Devilard, Elisabeth Fabre, Stéphanie Chabannon, Christian Xerri, Luc Farnarier, Catherine Cantoni, Claudia Bottino, Cristina Moretta, Alessandro Dubreuil, Patrice Lopez, Marc J Exp Med Article DNAX accessory molecule 1 (DNAM-1; CD226) is a transmembrane glycoprotein involved in T cell and natural killer (NK) cell cytotoxicity. We demonstrated recently that DNAM-1 triggers NK cell–mediated killing of tumor cells upon engagement by its two ligands, poliovirus receptor (PVR; CD155) and Nectin-2 (CD112). In the present paper, we show that PVR and Nectin-2 are expressed at cell junctions on primary vascular endothelial cells. Moreover, the specific binding of a soluble DNAM-1–Fc molecule was detected at endothelial junctions. This binding was almost completely abrogated by anti-PVR monoclonal antibodies (mAbs), but not modified by anti–Nectin-2 mAbs, which demonstrates that PVR is the major DNAM-1 ligand on endothelial cells. Because DNAM-1 is highly expressed on leukocytes, we investigated the role of the DNAM-1–PVR interaction during the monocyte transendothelial migration process. In vitro, both anti–DNAM-1 and anti-PVR mAbs strongly blocked the transmigration of monocytes through the endothelium. Moreover, after anti–DNAM-1 or anti-PVR mAb treatment, monocytes were arrested at the apical surface of the endothelium over intercellular junctions, which strongly suggests that the DNAM-1–PVR interaction occurs during the diapedesis step. Altogether, our results demonstrate that DNAM-1 regulates monocyte extravasation via its interaction with PVR expressed at endothelial junctions on normal cells. The Rockefeller University Press 2004-05-17 /pmc/articles/PMC2211807/ /pubmed/15136589 http://dx.doi.org/10.1084/jem.20032206 Text en Copyright © 2004, The Rockefeller University Press This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).
spellingShingle Article
Reymond, Nicolas
Imbert, Anne-Marie
Devilard, Elisabeth
Fabre, Stéphanie
Chabannon, Christian
Xerri, Luc
Farnarier, Catherine
Cantoni, Claudia
Bottino, Cristina
Moretta, Alessandro
Dubreuil, Patrice
Lopez, Marc
DNAM-1 and PVR Regulate Monocyte Migration through Endothelial Junctions
title DNAM-1 and PVR Regulate Monocyte Migration through Endothelial Junctions
title_full DNAM-1 and PVR Regulate Monocyte Migration through Endothelial Junctions
title_fullStr DNAM-1 and PVR Regulate Monocyte Migration through Endothelial Junctions
title_full_unstemmed DNAM-1 and PVR Regulate Monocyte Migration through Endothelial Junctions
title_short DNAM-1 and PVR Regulate Monocyte Migration through Endothelial Junctions
title_sort dnam-1 and pvr regulate monocyte migration through endothelial junctions
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2211807/
https://www.ncbi.nlm.nih.gov/pubmed/15136589
http://dx.doi.org/10.1084/jem.20032206
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