Vesicular stomatitis virus infection promotes immune evasion by preventing NKG2D-ligand surface expression.

Vesicular stomatitis virus infection promotes immune evasion by preventing NKG2D-ligand surface expression.

Vesicular stomatitis virus (VSV) has recently gained attention for its oncolytic ability in cancer treatment. Initially, we hypothesized that VSV infection could increase immune recognition of cancer cells through induction of the immune stimulatory NKG2D-ligands. Here we show that VSV infection lea...

Descripción completa

Guardado en:
Detalles Bibliográficos
Autores principales: Helle Jensen, Lars Andresen, Jens Nielsen, Jan Pravsgaard Christensen, Søren Skov
Formato: article
Lenguaje:EN
Publicado: Public Library of Science (PLoS) 2011
Materias:
Medicine
R
Science
Q
Acceso en línea:https://doaj.org/article/2713a62b59c74d7881c0a44827aae6a8
Etiquetas: Agregar Etiqueta
Sin Etiquetas, Sea el primero en etiquetar este registro!
id oai:doaj.org-article:2713a62b59c74d7881c0a44827aae6a8
record_format dspace
spelling oai:doaj.org-article:2713a62b59c74d7881c0a44827aae6a82021-11-18T06:48:25ZVesicular stomatitis virus infection promotes immune evasion by preventing NKG2D-ligand surface expression.1932-620310.1371/journal.pone.0023023https://doaj.org/article/2713a62b59c74d7881c0a44827aae6a82011-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/21857986/?tool=EBIhttps://doaj.org/toc/1932-6203Vesicular stomatitis virus (VSV) has recently gained attention for its oncolytic ability in cancer treatment. Initially, we hypothesized that VSV infection could increase immune recognition of cancer cells through induction of the immune stimulatory NKG2D-ligands. Here we show that VSV infection leads to a robust induction of MICA mRNA expression, however the subsequent surface expression is potently hindered. Thus, VSV lines up with human cytomegalovirus (HCMV) and adenovirus, which actively subvert the immune system by negatively affecting NKG2D-ligand surface expression. VSV infection caused an active suppression of NKG2D-ligand surface expression, affecting both endogenous and histone deacetylase (HDAC)-inhibitor induced MICA, MICB and ULBP-2 expression. The classical immune escape mechanism of VSV (i.e., the M protein blockade of nucleocytoplasmic mRNA transport) was not involved, as the VSV mutant strain, VSV(ΔM51), which possess a defective M protein, prevented MICA surface expression similarly to wild-type VSV. The VSV mediated down modulation of NKG2D-ligand expression did not involve apoptosis. Constitutive expression of MICA bypassed the escape mechanism, suggesting that VSV affect NKG2D-ligand expression at an early post-transcriptional level. Our results show that VSV possess an escape mechanism, which could affect the immune recognition of VSV infected cancer cells. This may also have implications for immune recognition of cancer cells after combined treatment with VSV and chemotherapeutic drugs.Helle JensenLars AndresenJens NielsenJan Pravsgaard ChristensenSøren SkovPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 6, Iss 8, p e23023 (2011)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Helle Jensen
Lars Andresen
Jens Nielsen
Jan Pravsgaard Christensen
Søren Skov
Vesicular stomatitis virus infection promotes immune evasion by preventing NKG2D-ligand surface expression.
description Vesicular stomatitis virus (VSV) has recently gained attention for its oncolytic ability in cancer treatment. Initially, we hypothesized that VSV infection could increase immune recognition of cancer cells through induction of the immune stimulatory NKG2D-ligands. Here we show that VSV infection leads to a robust induction of MICA mRNA expression, however the subsequent surface expression is potently hindered. Thus, VSV lines up with human cytomegalovirus (HCMV) and adenovirus, which actively subvert the immune system by negatively affecting NKG2D-ligand surface expression. VSV infection caused an active suppression of NKG2D-ligand surface expression, affecting both endogenous and histone deacetylase (HDAC)-inhibitor induced MICA, MICB and ULBP-2 expression. The classical immune escape mechanism of VSV (i.e., the M protein blockade of nucleocytoplasmic mRNA transport) was not involved, as the VSV mutant strain, VSV(ΔM51), which possess a defective M protein, prevented MICA surface expression similarly to wild-type VSV. The VSV mediated down modulation of NKG2D-ligand expression did not involve apoptosis. Constitutive expression of MICA bypassed the escape mechanism, suggesting that VSV affect NKG2D-ligand expression at an early post-transcriptional level. Our results show that VSV possess an escape mechanism, which could affect the immune recognition of VSV infected cancer cells. This may also have implications for immune recognition of cancer cells after combined treatment with VSV and chemotherapeutic drugs.
format article
author Helle Jensen
Lars Andresen
Jens Nielsen
Jan Pravsgaard Christensen
Søren Skov
author_facet Helle Jensen
Lars Andresen
Jens Nielsen
Jan Pravsgaard Christensen
Søren Skov
author_sort Helle Jensen
title Vesicular stomatitis virus infection promotes immune evasion by preventing NKG2D-ligand surface expression.
title_short Vesicular stomatitis virus infection promotes immune evasion by preventing NKG2D-ligand surface expression.
title_full Vesicular stomatitis virus infection promotes immune evasion by preventing NKG2D-ligand surface expression.
title_fullStr Vesicular stomatitis virus infection promotes immune evasion by preventing NKG2D-ligand surface expression.
title_full_unstemmed Vesicular stomatitis virus infection promotes immune evasion by preventing NKG2D-ligand surface expression.
title_sort vesicular stomatitis virus infection promotes immune evasion by preventing nkg2d-ligand surface expression.
publisher Public Library of Science (PLoS)
publishDate 2011
url https://doaj.org/article/2713a62b59c74d7881c0a44827aae6a8
work_keys_str_mv AT hellejensen vesicularstomatitisvirusinfectionpromotesimmuneevasionbypreventingnkg2dligandsurfaceexpression
AT larsandresen vesicularstomatitisvirusinfectionpromotesimmuneevasionbypreventingnkg2dligandsurfaceexpression
AT jensnielsen vesicularstomatitisvirusinfectionpromotesimmuneevasionbypreventingnkg2dligandsurfaceexpression
AT janpravsgaardchristensen vesicularstomatitisvirusinfectionpromotesimmuneevasionbypreventingnkg2dligandsurfaceexpression
AT sørenskov vesicularstomatitisvirusinfectionpromotesimmuneevasionbypreventingnkg2dligandsurfaceexpression
_version_ 1718424341653225472

Ejemplares similares