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Type I interferon receptor signalling is induced during demyelination while its function for myelin damage and repair is redundant

Schmidt, Hauke
Raasch, Jenni
Klinker, Florian
Krauss, Sandra
Bruck, Wolfgang
Prinz, Marco
Published in Experimental neurology. 2009, vol. 216, no. 2, p. 306-311
Abstract The type I interferons, interferon-beta and alpha (IFN-beta, IFN-alpha), are widely used for the treatment of autoimmune demyelination in the central nervous system (CNS). Their effects on de- and remyelination through the broadly expressed type I IFN receptor (IFNAR), however, are highly speculative. In order to elucidate the role of endogenous type I interferons for myelin damage and recovery we induced toxic demyelination in the absence of IFNAR1. We demonstrate that IFNAR signalling was induced during acute demyelination since the cytokine IFN-beta as well as the IFN-dependent genes IRF7, ISG15 and UBP43 were strongly upregulated. Myelin damage, astrocytic and microglia response, however, were not significantly reduced in the absence of IFNAR1. Furthermore, motor skills of IFNAR1-deficient animals during non-immune demyelination were unaltered. Finally, myelin recovery was found to be independent from endogenous IFNAR signalling, indicating a redundant role of this receptor for non-inflammatory myelin damage and repair.
Keywords AnimalsCentral Nervous System/metabolism/pathology/ultrastructureCuprizone/toxicityDemyelinating Diseases/chemically induced/*metabolism/pathology/*physiopathologyDisease Models, AnimalFemaleGene Expression Regulation/drug effects/geneticsGlial Fibrillary Acidic Protein/metabolismMiceMice, Inbred C57BLMice, KnockoutMotor Activity/drug effects/geneticsMotor Skills/physiologyMyelin Sheath/*metabolism/pathologyReceptor, Interferon alpha-beta/deficiency/genetics/*metabolismSignal Transduction/drug effects/*physiologySpecific Pathogen-Free Organisms
PMID: 19121307
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Research group La Sclérose en plaques (908)
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SCHMIDT, Hauke et al. Type I interferon receptor signalling is induced during demyelination while its function for myelin damage and repair is redundant. In: Experimental neurology, 2009, vol. 216, n° 2, p. 306-311. doi: 10.1016/j.expneurol.2008.12.002 https://archive-ouverte.unige.ch/unige:19098

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Deposited on : 2012-03-27

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