Cytomegalovirus m154 hinders CD48 cell-surface expression and promotes viral escape from host natural killer cell control.

Receptors of the signalling lymphocyte-activation molecules (SLAM) family are involved in the functional regulation of a variety of immune cells upon engagement through homotypic or heterotypic interactions amongst them. Here we show that murine cytomegalovirus (MCMV) dampens the surface expression...

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Autores principales:	Angela Zarama, Natàlia Pérez-Carmona, Domènec Farré, Adriana Tomic, Eva Maria Borst, Martin Messerle, Stipan Jonjic, Pablo Engel, Ana Angulo
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2014
Materias:	Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/448dfed7b07a479a9cd30b641559f83d
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spelling	oai:doaj.org-article:448dfed7b07a479a9cd30b641559f83d2021-11-18T06:06:50ZCytomegalovirus m154 hinders CD48 cell-surface expression and promotes viral escape from host natural killer cell control.1553-73661553-737410.1371/journal.ppat.1004000https://doaj.org/article/448dfed7b07a479a9cd30b641559f83d2014-03-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/24626474/?tool=EBIhttps://doaj.org/toc/1553-7366https://doaj.org/toc/1553-7374Receptors of the signalling lymphocyte-activation molecules (SLAM) family are involved in the functional regulation of a variety of immune cells upon engagement through homotypic or heterotypic interactions amongst them. Here we show that murine cytomegalovirus (MCMV) dampens the surface expression of several SLAM receptors during the course of the infection of macrophages. By screening a panel of MCMV deletion mutants, we identified m154 as an immunoevasin that effectively reduces the cell-surface expression of the SLAM family member CD48, a high-affinity ligand for natural killer (NK) and cytotoxic T cell receptor CD244. m154 is a mucin-like protein, expressed with early kinetics, which can be found at the cell surface of the infected cell. During infection, m154 leads to proteolytic degradation of CD48. This viral protein interferes with the NK cell cytotoxicity triggered by MCMV-infected macrophages. In addition, we demonstrate that an MCMV mutant virus lacking m154 expression results in an attenuated phenotype in vivo, which can be substantially restored after NK cell depletion in mice. This is the first description of a viral gene capable of downregulating CD48. Our novel findings define m154 as an important player in MCMV innate immune regulation.Angela ZaramaNatàlia Pérez-CarmonaDomènec FarréAdriana TomicAdriana TomicEva Maria BorstMartin MesserleStipan JonjicPablo EngelAna AnguloPublic Library of Science (PLoS)articleImmunologic diseases. AllergyRC581-607Biology (General)QH301-705.5ENPLoS Pathogens, Vol 10, Iss 3, p e1004000 (2014)
institution	DOAJ
collection	DOAJ
language	EN
topic	Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5
spellingShingle	Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5 Angela Zarama Natàlia Pérez-Carmona Domènec Farré Adriana Tomic Adriana Tomic Eva Maria Borst Martin Messerle Stipan Jonjic Pablo Engel Ana Angulo Cytomegalovirus m154 hinders CD48 cell-surface expression and promotes viral escape from host natural killer cell control.
description	Receptors of the signalling lymphocyte-activation molecules (SLAM) family are involved in the functional regulation of a variety of immune cells upon engagement through homotypic or heterotypic interactions amongst them. Here we show that murine cytomegalovirus (MCMV) dampens the surface expression of several SLAM receptors during the course of the infection of macrophages. By screening a panel of MCMV deletion mutants, we identified m154 as an immunoevasin that effectively reduces the cell-surface expression of the SLAM family member CD48, a high-affinity ligand for natural killer (NK) and cytotoxic T cell receptor CD244. m154 is a mucin-like protein, expressed with early kinetics, which can be found at the cell surface of the infected cell. During infection, m154 leads to proteolytic degradation of CD48. This viral protein interferes with the NK cell cytotoxicity triggered by MCMV-infected macrophages. In addition, we demonstrate that an MCMV mutant virus lacking m154 expression results in an attenuated phenotype in vivo, which can be substantially restored after NK cell depletion in mice. This is the first description of a viral gene capable of downregulating CD48. Our novel findings define m154 as an important player in MCMV innate immune regulation.
format	article
author	Angela Zarama Natàlia Pérez-Carmona Domènec Farré Adriana Tomic Adriana Tomic Eva Maria Borst Martin Messerle Stipan Jonjic Pablo Engel Ana Angulo
author_facet	Angela Zarama Natàlia Pérez-Carmona Domènec Farré Adriana Tomic Adriana Tomic Eva Maria Borst Martin Messerle Stipan Jonjic Pablo Engel Ana Angulo
author_sort	Angela Zarama
title	Cytomegalovirus m154 hinders CD48 cell-surface expression and promotes viral escape from host natural killer cell control.
title_short	Cytomegalovirus m154 hinders CD48 cell-surface expression and promotes viral escape from host natural killer cell control.
title_full	Cytomegalovirus m154 hinders CD48 cell-surface expression and promotes viral escape from host natural killer cell control.
title_fullStr	Cytomegalovirus m154 hinders CD48 cell-surface expression and promotes viral escape from host natural killer cell control.
title_full_unstemmed	Cytomegalovirus m154 hinders CD48 cell-surface expression and promotes viral escape from host natural killer cell control.
title_sort	cytomegalovirus m154 hinders cd48 cell-surface expression and promotes viral escape from host natural killer cell control.
publisher	Public Library of Science (PLoS)
publishDate	2014
url	https://doaj.org/article/448dfed7b07a479a9cd30b641559f83d
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Cytomegalovirus m154 hinders CD48 cell-surface expression and promotes viral escape from host natural killer cell control.

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