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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
(A) The biological activity of Human Recombinant IFN-beta was tested by its ability to inhibit the proliferation of TF-1 cells. Cell proliferation was measured using a fluorometric assay method. The EC50 is defined as the effective concentration of the growth factor at which cell proliferation is at 50% of maximum. The EC50 in the above example is less than 0.1 ng/mL.
(B) 2 μg of Human Recombinant IFN-beta was resolved with SDS-PAGE under reducing (+) and non-reducing (-) conditions and visualized by Coomassie Blue staining.
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