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Use Interferon beta (IFN-β) to modulate the activity of 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. Nat Rev Immunol, 2006). IFN-β binds to a receptor complex composed of IFNAR1 and IFNAR2, and initiates signal transduction via the JAK/STAT pathway. It is predominantly produced by fibroblasts, with smaller amounts from plasmocytoid dendritic cells. Macrophages and endothelial cells secrete IFN-β in response to viral infection (Reder & Feng. Front Immunol, 2013). IFN-β suppresses Th17 cells by affecting expression of IL-4, IL-10, and IL-27, and is a first-line treatment for multiple sclerosis. IFN-β was also shown to expand regulatory T cells and limit T cell trafficking to the central nervous system (Inoue & Shinohara. Immunology, 2013). Of the two IFN-β variants (IFN-β1 and IFN-β3), this product is the IFN-β1 form.
Subtype
Cytokines
Alternative Names
B cell interferon, Fibroblast interferon, IFNB1, Leukocyte interferon, Type I interferon
Cell Type
B Cells, Cancer Cells and Cell Lines, NK Cells, T Cells
Figure 1. Biological Activity and Molecular Mass of Human Recombinant IFN-beta (CHO-expressed)
(A) The biological activity of Human Recombinant IFN-beta (CHO-expressed) was tested in an antiviral assay using WISH cells infected with vesicular stomatitis virus. The EC50 in the above example is ≤ 20 pg/mL.
(B) Human Recombinant IFN-beta (CHO-expressed) was resolved with SDS-PAGE under reducing conditions. Human Recombinant G-CSF has a predicted molecular mass of 20 kDa.
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