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Cytomegalovirus immune evasion by perturbation of endosomal trafficking
Cytomegaloviruses (CMVs), members of the herpesvirus family, have evolved a variety of mechanisms to evade the immune response to survive in infected hosts and to establish latent infection. They effectively hide infected cells from the effector mechanisms of adaptive immunity by eliminating cellula...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4654299/ https://www.ncbi.nlm.nih.gov/pubmed/25263490 http://dx.doi.org/10.1038/cmi.2014.85 |
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author | Lučin, Pero Mahmutefendić, Hana Blagojević Zagorac, Gordana Ilić Tomaš, Maja |
author_facet | Lučin, Pero Mahmutefendić, Hana Blagojević Zagorac, Gordana Ilić Tomaš, Maja |
author_sort | Lučin, Pero |
collection | PubMed |
description | Cytomegaloviruses (CMVs), members of the herpesvirus family, have evolved a variety of mechanisms to evade the immune response to survive in infected hosts and to establish latent infection. They effectively hide infected cells from the effector mechanisms of adaptive immunity by eliminating cellular proteins (major histocompatibility Class I and Class II molecules) from the cell surface that display viral antigens to CD8 and CD4 T lymphocytes. CMVs also successfully escape recognition and elimination of infected cells by natural killer (NK) cells, effector cells of innate immunity, either by mimicking NK cell inhibitory ligands or by downregulating NK cell-activating ligands. To accomplish these immunoevasion functions, CMVs encode several proteins that function in the biosynthetic pathway by inhibiting the assembly and trafficking of cellular proteins that participate in immune recognition and thereby, block their appearance at the cell surface. However, elimination of these proteins from the cell surface can also be achieved by perturbation of their endosomal route and subsequent relocation from the cell surface into intracellular compartments. Namely, the physiological route of every cellular protein, including immune recognition molecules, is characterized by specific features that determine its residence time at the cell surface. In this review, we summarize the current understanding of endocytic trafficking of immune recognition molecules and perturbations of the endosomal system during infection with CMVs and other members of the herpesvirus family that contribute to their immune evasion mechanisms. |
format | Online Article Text |
id | pubmed-4654299 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-46542992015-12-04 Cytomegalovirus immune evasion by perturbation of endosomal trafficking Lučin, Pero Mahmutefendić, Hana Blagojević Zagorac, Gordana Ilić Tomaš, Maja Cell Mol Immunol Review Cytomegaloviruses (CMVs), members of the herpesvirus family, have evolved a variety of mechanisms to evade the immune response to survive in infected hosts and to establish latent infection. They effectively hide infected cells from the effector mechanisms of adaptive immunity by eliminating cellular proteins (major histocompatibility Class I and Class II molecules) from the cell surface that display viral antigens to CD8 and CD4 T lymphocytes. CMVs also successfully escape recognition and elimination of infected cells by natural killer (NK) cells, effector cells of innate immunity, either by mimicking NK cell inhibitory ligands or by downregulating NK cell-activating ligands. To accomplish these immunoevasion functions, CMVs encode several proteins that function in the biosynthetic pathway by inhibiting the assembly and trafficking of cellular proteins that participate in immune recognition and thereby, block their appearance at the cell surface. However, elimination of these proteins from the cell surface can also be achieved by perturbation of their endosomal route and subsequent relocation from the cell surface into intracellular compartments. Namely, the physiological route of every cellular protein, including immune recognition molecules, is characterized by specific features that determine its residence time at the cell surface. In this review, we summarize the current understanding of endocytic trafficking of immune recognition molecules and perturbations of the endosomal system during infection with CMVs and other members of the herpesvirus family that contribute to their immune evasion mechanisms. Nature Publishing Group 2015-03 2014-09-29 /pmc/articles/PMC4654299/ /pubmed/25263490 http://dx.doi.org/10.1038/cmi.2014.85 Text en Copyright © 2015 Chinese Society of Immunology and The University of Science and Technology http://creativecommons.org/licenses/by-nc-sa/3.0 This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 3.0 Unported License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-sa/3.0 |
spellingShingle | Review Lučin, Pero Mahmutefendić, Hana Blagojević Zagorac, Gordana Ilić Tomaš, Maja Cytomegalovirus immune evasion by perturbation of endosomal trafficking |
title | Cytomegalovirus immune evasion by perturbation of endosomal trafficking |
title_full | Cytomegalovirus immune evasion by perturbation of endosomal trafficking |
title_fullStr | Cytomegalovirus immune evasion by perturbation of endosomal trafficking |
title_full_unstemmed | Cytomegalovirus immune evasion by perturbation of endosomal trafficking |
title_short | Cytomegalovirus immune evasion by perturbation of endosomal trafficking |
title_sort | cytomegalovirus immune evasion by perturbation of endosomal trafficking |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4654299/ https://www.ncbi.nlm.nih.gov/pubmed/25263490 http://dx.doi.org/10.1038/cmi.2014.85 |
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