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• W1963535932 abstract "The type I interferons, interferon-beta and alpha (IFN-β, IFN-α), 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-β 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." @default.
• W1963535932 created "2016-06-24" @default.
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• W1963535932 date "2009-04-01" @default.
• W1963535932 modified "2023-10-17" @default.
• W1963535932 title "Type I interferon receptor signalling is induced during demyelination while its function for myelin damage and repair is redundant" @default.
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• W1963535932 doi "https://doi.org/10.1016/j.expneurol.2008.12.002" @default.
• W1963535932 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/19121307" @default.
• W1963535932 hasPublicationYear "2009" @default.
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