Human endogenous retrovirus protein activates innate immunity and promotes experimental allergic encephalomyelitis in mice.

Multiple sclerosis (MS) is a complex multifactorial disease of the central nervous system (CNS) for which animal models have mainly addressed downstream immunopathology but not potential inducers of autoimmunity. In the absence of a pathogen known to cause neuroinflammation in MS, Mycobacterial lysa...

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Autores principales: Hervé Perron, Hei-Lanne Dougier-Reynaud, Christina Lomparski, Iuliana Popa, Reza Firouzi, Jean-Baptiste Bertrand, Suzana Marusic, Jacques Portoukalian, Evelyne Jouvin-Marche, Christian L Villiers, Jean-Louis Touraine, Patrice N Marche
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Publicado: Public Library of Science (PLoS) 2013
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spelling oai:doaj.org-article:32f3919b696a4600af910addc64f022e2021-11-18T08:43:12ZHuman endogenous retrovirus protein activates innate immunity and promotes experimental allergic encephalomyelitis in mice.1932-620310.1371/journal.pone.0080128https://doaj.org/article/32f3919b696a4600af910addc64f022e2013-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/24324591/?tool=EBIhttps://doaj.org/toc/1932-6203Multiple sclerosis (MS) is a complex multifactorial disease of the central nervous system (CNS) for which animal models have mainly addressed downstream immunopathology but not potential inducers of autoimmunity. In the absence of a pathogen known to cause neuroinflammation in MS, Mycobacterial lysate is commonly used in the form of complete Freund's adjuvant to induce autoimmunity to myelin proteins in Experimental Allergic Encephalomyelitis (EAE), an animal model for MS. The present study demonstrates that a protein from the human endogenous retrovirus HERV-W family (MSRV-Env) can be used instead of mycobacterial lysate to induce autoimmunity and EAE in mice injected with MOG, with typical anti-myelin response and CNS lesions normally seen in this model. MSRV-Env was shown to induce proinflammatory response in human macrophage cells through TLR4 activation pathway. The present results demonstrate a similar activation of murine dendritic cells and show the ability of MSRV-Env to trigger EAE in mice. In previous studies, MSRV-Env protein was reproducibly detected in MS brain lesions within microglia and perivascular macrophages. The present results are therefore likely to provide a model for MS, in which the upstream adjuvant triggering neuroinflammation is the one detected in MS active lesions. This model now allows pre-clinical studies with therapeutic agents targeting this endogenous retroviral protein in MS.Hervé PerronHei-Lanne Dougier-ReynaudChristina LomparskiIuliana PopaReza FirouziJean-Baptiste BertrandSuzana MarusicJacques PortoukalianEvelyne Jouvin-MarcheChristian L VilliersJean-Louis TourainePatrice N MarchePublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 8, Iss 12, p e80128 (2013)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Hervé Perron
Hei-Lanne Dougier-Reynaud
Christina Lomparski
Iuliana Popa
Reza Firouzi
Jean-Baptiste Bertrand
Suzana Marusic
Jacques Portoukalian
Evelyne Jouvin-Marche
Christian L Villiers
Jean-Louis Touraine
Patrice N Marche
Human endogenous retrovirus protein activates innate immunity and promotes experimental allergic encephalomyelitis in mice.
description Multiple sclerosis (MS) is a complex multifactorial disease of the central nervous system (CNS) for which animal models have mainly addressed downstream immunopathology but not potential inducers of autoimmunity. In the absence of a pathogen known to cause neuroinflammation in MS, Mycobacterial lysate is commonly used in the form of complete Freund's adjuvant to induce autoimmunity to myelin proteins in Experimental Allergic Encephalomyelitis (EAE), an animal model for MS. The present study demonstrates that a protein from the human endogenous retrovirus HERV-W family (MSRV-Env) can be used instead of mycobacterial lysate to induce autoimmunity and EAE in mice injected with MOG, with typical anti-myelin response and CNS lesions normally seen in this model. MSRV-Env was shown to induce proinflammatory response in human macrophage cells through TLR4 activation pathway. The present results demonstrate a similar activation of murine dendritic cells and show the ability of MSRV-Env to trigger EAE in mice. In previous studies, MSRV-Env protein was reproducibly detected in MS brain lesions within microglia and perivascular macrophages. The present results are therefore likely to provide a model for MS, in which the upstream adjuvant triggering neuroinflammation is the one detected in MS active lesions. This model now allows pre-clinical studies with therapeutic agents targeting this endogenous retroviral protein in MS.
format article
author Hervé Perron
Hei-Lanne Dougier-Reynaud
Christina Lomparski
Iuliana Popa
Reza Firouzi
Jean-Baptiste Bertrand
Suzana Marusic
Jacques Portoukalian
Evelyne Jouvin-Marche
Christian L Villiers
Jean-Louis Touraine
Patrice N Marche
author_facet Hervé Perron
Hei-Lanne Dougier-Reynaud
Christina Lomparski
Iuliana Popa
Reza Firouzi
Jean-Baptiste Bertrand
Suzana Marusic
Jacques Portoukalian
Evelyne Jouvin-Marche
Christian L Villiers
Jean-Louis Touraine
Patrice N Marche
author_sort Hervé Perron
title Human endogenous retrovirus protein activates innate immunity and promotes experimental allergic encephalomyelitis in mice.
title_short Human endogenous retrovirus protein activates innate immunity and promotes experimental allergic encephalomyelitis in mice.
title_full Human endogenous retrovirus protein activates innate immunity and promotes experimental allergic encephalomyelitis in mice.
title_fullStr Human endogenous retrovirus protein activates innate immunity and promotes experimental allergic encephalomyelitis in mice.
title_full_unstemmed Human endogenous retrovirus protein activates innate immunity and promotes experimental allergic encephalomyelitis in mice.
title_sort human endogenous retrovirus protein activates innate immunity and promotes experimental allergic encephalomyelitis in mice.
publisher Public Library of Science (PLoS)
publishDate 2013
url https://doaj.org/article/32f3919b696a4600af910addc64f022e
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