

Other version: http://www.sciencedirect.com/science/article/pii/S0014488608004718
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Type I interferon receptor signalling is induced during demyelination while its function for myelin damage and repair is redundant |
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Authors | ||
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 | Animals — Central Nervous System/metabolism/pathology/ultrastructure — Cuprizone/toxicity — Demyelinating Diseases/chemically induced/*metabolism/pathology/*physiopathology — Disease Models, Animal — Female — Gene Expression Regulation/drug effects/genetics — Glial Fibrillary Acidic Protein/metabolism — Mice — Mice, Inbred C57BL — Mice, Knockout — Motor Activity/drug effects/genetics — Motor Skills/physiology — Myelin Sheath/*metabolism/pathology — Receptor, Interferon alpha-beta/deficiency/genetics/*metabolism — Signal Transduction/drug effects/*physiology — Specific Pathogen-Free Organisms | |
Identifiers | PMID: 19121307 | |
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![]() ![]() Other version: http://www.sciencedirect.com/science/article/pii/S0014488608004718 |
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Structures | ||
Research group | La Sclérose en plaques (908) | |
Citation (ISO format) | 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 |