| First Author | Schmidt H | Year | 2009 |
| Journal | Exp Neurol | Volume | 216 |
| Issue | 2 | Pages | 306-11 |
| PubMed ID | 19121307 | Mgi Jnum | J:147309 |
| Mgi Id | MGI:3840049 | Doi | 10.1016/j.expneurol.2008.12.002 |
| Citation | Schmidt H, et al. (2009) Type I interferon receptor signalling is induced during demyelination while its function for myelin damage and repair is redundant. Exp Neurol 216(2):306-11 |
| abstractText | 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. |
