Scientific article

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

Published inExperimental neurology, vol. 216, no. 2, p. 306-311
Publication date2009

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.

  • 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
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
Updates (1)
ISSN of the journal0014-4886

Technical informations

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