Abstract
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.
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