Type I interferon receptor signalling is induced during demyelination while its function for myelin damage and repair is redundant |
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Authors: | Hauke Schmidt, Jenni Raasch, Doron Merkler, Florian Klinker, Sandra Krauss, Wolfgang Brü ck,Marco Prinz, |
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Affiliation: | aInstitute of Neuropathology, University Medical Center, Georg August University, Göttingen, Germany;bDepartment of Clinical Neurophysiology, Georg-August-University of Göttingen, Germany;cDepartment of Neuropathology, University of Freiburg, Breisacher Str. 64, D-79106 Freiburg, Germany;dInstitute for Multiple Sclerosis Research, Gemeinnützige Hertie-Stiftung und University Medical Center, Georg August University, Göttingen, Germany |
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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. |
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Keywords: | Demyelination Remyelination Interferons Multiple sclerosis |
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