Lack of interferon-beta leads to accelerated remyelination in a toxic model of central nervous system demyelination.

2.50
Hdl Handle:
http://hdl.handle.net/10033/25153
Title:
Lack of interferon-beta leads to accelerated remyelination in a toxic model of central nervous system demyelination.
Authors:
Trebst, Corinna; Heine, Sandra; Lienenklaus, Stefan; Lindner, Maren; Baumgärtner, Wolfgang; Weiss, Siegfried; Stangel, Martin
Abstract:
Interferon-beta (IFN-beta) is a pleiotropic cytokine that is known to modulate the immune response in multiple sclerosis (MS), an inflammatory demyelinating disease of the central nervous system (CNS). Spontaneous remyelination and repair mechanisms in MS are mostly insufficient and contribute to clinical disability. Here, we investigated whether IFN-beta has a potential in modifying the extent of de- and remyelination in a toxic model of CNS demyelination induced by the copper chelator cuprizone. IFN-beta deficient (k/o) mice showed an accelerated spontaneous remyelination. However, the amount of remyelination after 6 weeks did not differ between the two groups. Demyelination in IFN-beta k/o mice was paralleled by a diminished astrocytic and microglia response as compared with wildtype controls, whereas the accelerated remyelination was paralleled by an increased number of oligodendrocyte precursor cells (OPC) within the demyelinated lesion at the beginning of the remyelination phase. We hypothesize that the absence of IFN-beta leads to more efficient recruitment and proliferation of OPC already during demyelination, thus allowing early remyelination. These results demonstrate that IFN-beta is able to alter remyelination in the absence of an immune-mediated demyelination.
Affiliation:
Department of Neurology, Medical School Hannover, Carl-Neuberg-Str. 1, 30625, Hannover, Germany.
Citation:
Lack of interferon-beta leads to accelerated remyelination in a toxic model of central nervous system demyelination. 2007, 114 (6):587-96 Acta Neuropathol.
Journal:
Acta neuropathologica
Issue Date:
Dec-2007
URI:
http://hdl.handle.net/10033/25153
DOI:
10.1007/s00401-007-0300-z
PubMed ID:
17940777
Type:
Article
Language:
en
ISSN:
0001-6322
Appears in Collections:
Publications of RG Mucosal Immunity (MI)

Full metadata record

DC FieldValue Language
dc.contributor.authorTrebst, Corinna-
dc.contributor.authorHeine, Sandra-
dc.contributor.authorLienenklaus, Stefan-
dc.contributor.authorLindner, Maren-
dc.contributor.authorBaumgärtner, Wolfgang-
dc.contributor.authorWeiss, Siegfried-
dc.contributor.authorStangel, Martin-
dc.date.accessioned2008-05-08T14:10:16Z-
dc.date.available2008-05-08T14:10:16Z-
dc.date.issued2007-12-
dc.identifier.citationLack of interferon-beta leads to accelerated remyelination in a toxic model of central nervous system demyelination. 2007, 114 (6):587-96 Acta Neuropathol.en
dc.identifier.issn0001-6322-
dc.identifier.pmid17940777-
dc.identifier.doi10.1007/s00401-007-0300-z-
dc.identifier.urihttp://hdl.handle.net/10033/25153-
dc.description.abstractInterferon-beta (IFN-beta) is a pleiotropic cytokine that is known to modulate the immune response in multiple sclerosis (MS), an inflammatory demyelinating disease of the central nervous system (CNS). Spontaneous remyelination and repair mechanisms in MS are mostly insufficient and contribute to clinical disability. Here, we investigated whether IFN-beta has a potential in modifying the extent of de- and remyelination in a toxic model of CNS demyelination induced by the copper chelator cuprizone. IFN-beta deficient (k/o) mice showed an accelerated spontaneous remyelination. However, the amount of remyelination after 6 weeks did not differ between the two groups. Demyelination in IFN-beta k/o mice was paralleled by a diminished astrocytic and microglia response as compared with wildtype controls, whereas the accelerated remyelination was paralleled by an increased number of oligodendrocyte precursor cells (OPC) within the demyelinated lesion at the beginning of the remyelination phase. We hypothesize that the absence of IFN-beta leads to more efficient recruitment and proliferation of OPC already during demyelination, thus allowing early remyelination. These results demonstrate that IFN-beta is able to alter remyelination in the absence of an immune-mediated demyelination.en
dc.language.isoenen
dc.subject.meshAnimalsen
dc.subject.meshAstrocytesen
dc.subject.meshAxonsen
dc.subject.meshChelating Agentsen
dc.subject.meshCuprizoneen
dc.subject.meshDisease Models, Animalen
dc.subject.meshGliosisen
dc.subject.meshInterferon-betaen
dc.subject.meshMaleen
dc.subject.meshMiceen
dc.subject.meshMice, Inbred C57BLen
dc.subject.meshMice, Knockouten
dc.subject.meshMicrogliaen
dc.subject.meshMicroscopy, Electron, Transmissionen
dc.subject.meshMultiple Sclerosisen
dc.subject.meshMyelin Sheathen
dc.subject.meshRecovery of Functionen
dc.titleLack of interferon-beta leads to accelerated remyelination in a toxic model of central nervous system demyelination.en
dc.typeArticleen
dc.contributor.departmentDepartment of Neurology, Medical School Hannover, Carl-Neuberg-Str. 1, 30625, Hannover, Germany.en
dc.identifier.journalActa neuropathologicaen

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