IFN-β1 is part of the type I IFN multigene family which includes at least eight subclases: IFN-α, IFN-β, IFN-ε, IFN-κ, IFN-ω, IFN-τ, IFN-δ, and IFN-ζ (limitin). Type I interferons (IFNs) (alpha/beta interferon [IFN-α/β]) are expressed as a first line of defense against viruses and play a critical role in the antiviral response. The antiviral activity of type I IFNs is exerted by different mechanisms, e.g. blockage of viral entry into the cell, control of viral transcription, cleavage of RNA, and preventing translation; therefore, type I IFNs block virus replication. In addition, type I INFs modulate the innate and adaptive immune responses. IFN-α/β induces natural killer cell cytotoxicity and expression of major histocompatibility complex class I on most cells and costimulatory molecules on antigen-presenting cells. Also, type I interferons act directly on CD8 T cells to allow clonal expansion and memory formation in response to viral infection. Plasmacytoid dendritic cells (pDCs) produce high amounts of type I interferons (IFNs) and a variety of inflammatory cytokines and chemokines in response to viral infections. Mice deficient for IFN-β type I IFN receptor (IFNAR) have demonstrated an increased susceptibility to experimental autoimmune encephalomyelitis (EAE). Animal studies have shown that neutralization of IL-23 or the lack of IL-23 p19 gene expression completely ameliorated EAE. These data correlate with the fact that IFN-β has been used in the treatment of multiple sclerosis (MS) in humans, and it has been suggested that IFN-β inhibits human Th17 cell differentiation. It is known that Th17 cells play a central role in the immunopathogenesis of MS, and IL-23 plays a role in the expansion of differentiated TL17 cells in mice and differentiation of Th17 cells in humans.