Mouse Interferon-Beta (IFN-β) is a type I interferon produced primarily by virus-infected epithelial cells, fibroblasts, macrophages, and dendritic cells in mice (Mus musculus), where it serves as a critical early mediator of innate antiviral immunity. Following recognition of viral RNA or DNA by pattern recognition receptors such as RIG-I, MDA5, and the cGAS-STING pathway, murine IFN-β is rapidly induced and signals through the type I interferon receptor complex (IFNAR1/IFNAR2), activating JAK/STAT signaling and driving expression of interferon-stimulated genes (ISGs) that inhibit viral replication, enhance antigen presentation, and promote natural killer (NK) cell activation and adaptive immune responses. Mouse IFN-β plays a central role in experimental models of viral infections including influenza virus, lymphocytic choriomeningitis virus (LCMV), murine cytomegalovirus (MCMV), West Nile virus, and SARS-CoV-2 (adapted strains), where the timing and magnitude of IFN-β production influence viral control and immunopathology. IFN-β is also critically involved in models of autoimmune disease, particularly experimental autoimmune encephalomyelitis (EAE), where it has immunomodulatory effects similar to its therapeutic use in human multiple sclerosis. IFNAR-deficient and IFN-β knockout mouse models have been instrumental in defining type I interferon signaling pathways, antiviral defense mechanisms, and interferon-driven inflammation. As both a biomarker and functional regulator of innate immunity, murine IFN-β remains central to preclinical research on antiviral therapies, vaccine development, cancer immunology, and immune-mediated disease.