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Title

Type I interferon receptor signalling is induced during demyelination while its function for myelin damage and repair is redundant
Authors
Schmidt, Hauke
Raasch, Jenni
Merkler, Doron
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 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
Full text
Article - document accessible for UNIGE members only Limited access to UNIGE
Other version: http://www.sciencedirect.com/science/article/pii/S0014488608004718
Structures
Faculté de médecine / Section de médecine fondamentale / Département de pathologie et immunologie
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

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Deposited on : 2012-03-27

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