Induction of type I interferon in the central nervous system plays a protective role in EAE

      Interferon-β (IFN-β) is used to treat patients with Multiple sclerosis (MS). IFN-β is a member of the type I IFN family, which shares a common receptor (IFNAR), and is induced by stimulation of innate receptors. Type I IFN are increased in the CNS during experimental autoimmune encephalomyelitis (EAE), an animal model for MS, and lack of IFN-β and type I IFN signalling worsen EAE, suggesting an important role for endogenous IFN-β in the CNS. The aim of this study was to identify the role of endogenous type I IFN in the CNS. Mice were administered poly I:C into the cerebrospinal fluid via the cisterna magna and induction of IFN-β was demonstrated by in vivo imaging of a luciferase/IFN-β reporter mouse. Intrathecal administration of poly I:C transiently induced IFN-β in the brain and spinal cord. EAE was induced in C57BL/6 and IFNAR-deficient mice by immunization with myelin oligodendrocyte glycoprotein 35–55. At onset of EAE, mice received a single intrathecal injection of poly I:C. This transiently prevented EAE progression. In contrast, intrathecal administration of poly I:C had no effect on progression of EAE in IFNAR-deficient mice, indicating type I IFN mediated poly I:C induced suppression of EAE. These results suggest that type I IFN induced within the CNS plays a protective role in EAE. This underscores the role of endogenous type I IFN in mediating neuroprotection.
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