Canine Interferon-Beta (IFN-β) is a type I interferon produced primarily by virus-infected epithelial cells, fibroblasts, macrophages, and dendritic cells in dogs (Canis lupus familiaris), where it functions as a key early mediator of innate antiviral immunity. Following recognition of viral nucleic acids by pattern recognition receptors such as RIG-I–like receptors and the cGAS-STING pathway, canine 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 activation of natural killer (NK) cells and adaptive immune responses. IFN-β is critically involved in host defense against viral pathogens such as canine parvovirus, canine distemper virus, canine influenza virus, and canine adenovirus, and the magnitude and timing of IFN-β responses can influence disease severity and viral clearance. Dysregulated type I interferon signaling has also been implicated in immune-mediated diseases and inflammatory conditions in dogs. In veterinary and translational research, characterization of canine IFN-β supports studies of antiviral immunity, vaccine development, autoimmune disease mechanisms, and comparative interferon biology, particularly as dogs serve as valuable spontaneous models for human infectious, inflammatory, and immune-mediated diseases.