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Human IFN-beta is a type I interferon, normally produced by fibroblasts, involved mainly in innate immune response, with antiviral and antiproliferative effects. It is considered first-line therapy for management of MS because of its immunomodulatory properties. It downregulates HLA class II molecules in antigen presenting cells. It also upregulates the expression of PDL-2 inhibitory molecules, which interact with their respective receptors on the T cells and induce apoptosis. It also inhibits proliferation of macrophages and so activation of autoreactive T cells.
The IFN-beta gene was cloned from human fibroblasts and altered to substitute Serine for the Cysteine residue found at position 17.