Detrimental contribution of the immuno-inhibitor B7-H1 to rabies virus encephalitis
Rabies virus is the etiological agent of an acute encephalitis, which in absence of post exposure treatment is fatal in almost all cases. Virus lethality rests on its ability to evade the immune response. In this study, we analyzed the role of the immuno-inhibitory molecule B7-H1 in this virus strat...
- Autores:
-
Lafon, Monique
Mégret, Françoise
Meuth, Sven G.
Simon, Ole
Velandia-Romero, Myriam Lucía
Lafage, Mireille
Chen, Lieping
Alexopoulou, Lena
Flavell, Richard A.
Prehaud, Prehaud
Wiendl, Heinz
- Tipo de recurso:
- Article of journal
- Fecha de publicación:
- 2008
- Institución:
- Universidad El Bosque
- Repositorio:
- Repositorio U. El Bosque
- Idioma:
- eng
- OAI Identifier:
- oai:repositorio.unbosque.edu.co:20.500.12495/3894
- Acceso en línea:
- http://hdl.handle.net/20.500.12495/3894
https://doi.org/10.4049/jimmunol.180.11.7506
https://repositorio.unbosque.edu.co
- Palabra clave:
- Virus de la rabia
Virus ARN
Virus de la encefalitis
- Rights
- openAccess
- License
- Acceso abierto
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Repositorio U. El Bosque |
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|
dc.title.spa.fl_str_mv |
Detrimental contribution of the immuno-inhibitor B7-H1 to rabies virus encephalitis |
dc.title.translated.spa.fl_str_mv |
Detrimental contribution of the immuno-inhibitor B7-H1 to rabies virus encephalitis |
title |
Detrimental contribution of the immuno-inhibitor B7-H1 to rabies virus encephalitis |
spellingShingle |
Detrimental contribution of the immuno-inhibitor B7-H1 to rabies virus encephalitis Virus de la rabia Virus ARN Virus de la encefalitis |
title_short |
Detrimental contribution of the immuno-inhibitor B7-H1 to rabies virus encephalitis |
title_full |
Detrimental contribution of the immuno-inhibitor B7-H1 to rabies virus encephalitis |
title_fullStr |
Detrimental contribution of the immuno-inhibitor B7-H1 to rabies virus encephalitis |
title_full_unstemmed |
Detrimental contribution of the immuno-inhibitor B7-H1 to rabies virus encephalitis |
title_sort |
Detrimental contribution of the immuno-inhibitor B7-H1 to rabies virus encephalitis |
dc.creator.fl_str_mv |
Lafon, Monique Mégret, Françoise Meuth, Sven G. Simon, Ole Velandia-Romero, Myriam Lucía Lafage, Mireille Chen, Lieping Alexopoulou, Lena Flavell, Richard A. Prehaud, Prehaud Wiendl, Heinz |
dc.contributor.author.none.fl_str_mv |
Lafon, Monique Mégret, Françoise Meuth, Sven G. Simon, Ole Velandia-Romero, Myriam Lucía Lafage, Mireille Chen, Lieping Alexopoulou, Lena Flavell, Richard A. Prehaud, Prehaud Wiendl, Heinz |
dc.contributor.orcid.none.fl_str_mv |
Velandia-Romero, Myriam Lucía [0000-0002-3340-7304] |
dc.subject.decs.spa.fl_str_mv |
Virus de la rabia Virus ARN Virus de la encefalitis |
topic |
Virus de la rabia Virus ARN Virus de la encefalitis |
description |
Rabies virus is the etiological agent of an acute encephalitis, which in absence of post exposure treatment is fatal in almost all cases. Virus lethality rests on its ability to evade the immune response. In this study, we analyzed the role of the immuno-inhibitory molecule B7-H1 in this virus strategy. We showed that in the brain and spinal cord of mice, rabies virus infection resulted in significant up-regulation of B7-H1 expression, which is specifically expressed in infected neurons. Correlatively, clinical rabies in B7-H1−/− mice is markedly less severe than in wild-type mice. B7-H1−/− mice display resistance to rabies. Virus invasion is reduced and the level of migratory CD8 T cells increases into the nervous system, while CD4/CD8 ratio remains unchanged in the periphery. In vivo, neuronal B7-H1 expression is critically depending on TLR3 signaling and IFN-β, because TLR3−/− mice—in which IFN-β production is reduced—showed only a limited increase of B7-H1 transcripts after infection. These data provide evidence that neurons can express the B7-H1 molecule after viral stress or exposure to a particular cytokine environment. They show that the B7-H1/PD-1 pathway can be exploited locally and in an organ specific manner—here the nervous system—by a neurotropic virus to promote successful host invasion. |
publishDate |
2008 |
dc.date.issued.none.fl_str_mv |
2008 |
dc.date.accessioned.none.fl_str_mv |
2020-08-31T11:19:22Z |
dc.date.available.none.fl_str_mv |
2020-08-31T11:19:22Z |
dc.type.coar.fl_str_mv |
http://purl.org/coar/resource_type/c_2df8fbb1 |
dc.type.coarversion.fl_str_mv |
http://purl.org/coar/version/c_970fb48d4fbd8a85 |
dc.type.local.none.fl_str_mv |
Artículo de revista |
dc.type.coar.none.fl_str_mv |
http://purl.org/coar/resource_type/c_6501 |
dc.type.driver.none.fl_str_mv |
info:eu-repo/semantics/article |
format |
http://purl.org/coar/resource_type/c_6501 |
dc.identifier.issn.none.fl_str_mv |
1550-6606 |
dc.identifier.uri.none.fl_str_mv |
http://hdl.handle.net/20.500.12495/3894 |
dc.identifier.doi.none.fl_str_mv |
https://doi.org/10.4049/jimmunol.180.11.7506 |
dc.identifier.instname.spa.fl_str_mv |
instname:Universidad El Bosque |
dc.identifier.reponame.spa.fl_str_mv |
reponame:Repositorio Institucional Universidad El Bosque |
dc.identifier.repourl.none.fl_str_mv |
https://repositorio.unbosque.edu.co |
identifier_str_mv |
1550-6606 instname:Universidad El Bosque reponame:Repositorio Institucional Universidad El Bosque |
url |
http://hdl.handle.net/20.500.12495/3894 https://doi.org/10.4049/jimmunol.180.11.7506 https://repositorio.unbosque.edu.co |
dc.language.iso.none.fl_str_mv |
eng |
language |
eng |
dc.relation.ispartofseries.spa.fl_str_mv |
The Journal of Immunology, 1550-6606, Vol. 180, Nro. 11, 2008 p. 7506-7515 |
dc.relation.uri.none.fl_str_mv |
https://www.jimmunol.org/content/180/11/7506.long |
dc.rights.local.spa.fl_str_mv |
Acceso abierto |
dc.rights.accessrights.none.fl_str_mv |
http://purl.org/coar/access_right/c_abf2 info:eu-repo/semantics/openAccess Acceso abierto |
dc.rights.creativecommons.none.fl_str_mv |
2008-06 |
rights_invalid_str_mv |
Acceso abierto http://purl.org/coar/access_right/c_abf2 2008-06 |
eu_rights_str_mv |
openAccess |
dc.format.mimetype.none.fl_str_mv |
application/pdf |
dc.publisher.spa.fl_str_mv |
The American Association of Immunologists |
dc.publisher.journal.spa.fl_str_mv |
The Journal of Immunology |
institution |
Universidad El Bosque |
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Lafon, MoniqueMégret, FrançoiseMeuth, Sven G.Simon, OleVelandia-Romero, Myriam LucíaLafage, MireilleChen, LiepingAlexopoulou, LenaFlavell, Richard A.Prehaud, PrehaudWiendl, HeinzVelandia-Romero, Myriam Lucía [0000-0002-3340-7304]2020-08-31T11:19:22Z2020-08-31T11:19:22Z20081550-6606http://hdl.handle.net/20.500.12495/3894https://doi.org/10.4049/jimmunol.180.11.7506instname:Universidad El Bosquereponame:Repositorio Institucional Universidad El Bosquehttps://repositorio.unbosque.edu.coapplication/pdfengThe American Association of ImmunologistsThe Journal of ImmunologyThe Journal of Immunology, 1550-6606, Vol. 180, Nro. 11, 2008 p. 7506-7515https://www.jimmunol.org/content/180/11/7506.longDetrimental contribution of the immuno-inhibitor B7-H1 to rabies virus encephalitisDetrimental contribution of the immuno-inhibitor B7-H1 to rabies virus encephalitisArtículo de revistahttp://purl.org/coar/resource_type/c_6501http://purl.org/coar/resource_type/c_2df8fbb1info:eu-repo/semantics/articlehttp://purl.org/coar/version/c_970fb48d4fbd8a85Virus de la rabiaVirus ARNVirus de la encefalitisRabies virus is the etiological agent of an acute encephalitis, which in absence of post exposure treatment is fatal in almost all cases. Virus lethality rests on its ability to evade the immune response. In this study, we analyzed the role of the immuno-inhibitory molecule B7-H1 in this virus strategy. We showed that in the brain and spinal cord of mice, rabies virus infection resulted in significant up-regulation of B7-H1 expression, which is specifically expressed in infected neurons. Correlatively, clinical rabies in B7-H1−/− mice is markedly less severe than in wild-type mice. B7-H1−/− mice display resistance to rabies. Virus invasion is reduced and the level of migratory CD8 T cells increases into the nervous system, while CD4/CD8 ratio remains unchanged in the periphery. In vivo, neuronal B7-H1 expression is critically depending on TLR3 signaling and IFN-β, because TLR3−/− mice—in which IFN-β production is reduced—showed only a limited increase of B7-H1 transcripts after infection. These data provide evidence that neurons can express the B7-H1 molecule after viral stress or exposure to a particular cytokine environment. They show that the B7-H1/PD-1 pathway can be exploited locally and in an organ specific manner—here the nervous system—by a neurotropic virus to promote successful host invasion.Acceso abiertohttp://purl.org/coar/access_right/c_abf2info:eu-repo/semantics/openAccessAcceso abierto2008-06ORIGINALLafon_Monique_2008.pdfLafon_Monique_2008.pdfapplication/pdf444564https://repositorio.unbosque.edu.co/bitstreams/4761bc92-e607-471f-9c16-2dab39b6c79e/downloadd08c869082870202cbc630eb6e2629a8MD51LICENSElicense.txtlicense.txttext/plain; charset=utf-81748https://repositorio.unbosque.edu.co/bitstreams/bead27b9-a741-4a7c-84ae-3ea422c5ba31/download8a4605be74aa9ea9d79846c1fba20a33MD52THUMBNAILLafon_Monique_2008.pdf.jpgLafon_Monique_2008.pdf.jpgimage/jpeg5775https://repositorio.unbosque.edu.co/bitstreams/c8655b55-7484-4cc1-a85b-4357f69b2164/download7210a811635d1799e7c05fee5d259be7MD53TEXTLafon_Monique_2008.pdf.txtLafon_Monique_2008.pdf.txtExtracted texttext/plain58715https://repositorio.unbosque.edu.co/bitstreams/f6ffba47-1ed7-4b5a-a3c4-192463214c22/download64ef51c2072e276c55d6b75519a55944MD5420.500.12495/3894oai:repositorio.unbosque.edu.co:20.500.12495/38942024-02-06 23:41:54.015restrictedhttps://repositorio.unbosque.edu.coRepositorio Institucional Universidad El Bosquebibliotecas@biteca.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 |