Human Recombinant IFN-beta

Interferon beta (IFN-β), also known as type I interferon, is produced by fibroblasts, and in smaller amounts by plasmocytoid dendritic cells. Macrophages and endothelial cells secrete IFN-β in response to a viral infection (Reder & Feng). IFN-β binds to a receptor complex composed of IFNAR1 and IFNAR2, and initiates signal transduction via the JAK/STAT pathway; this culminates in the transcription and activation of many genes that control dendritic cell activation, T cell survival, NK cell activation, chemokine expression, lymph node retention, and antiproliferative and antiviral effects (Dunn et al.). IFN-β is a first-line treatment for multiple sclerosis. It suppresses Th17 cells by affecting expression of IL-4, IL-10, and IL-27. IFN-β was also shown to expand regulatory T cells and limit T cell trafficking to the central nervous system (Inoue & Shinohara). Out of the two variants of IFN-β (IFN-β1 and IFN-β3), this product is the IFN-β1 form.