Mouse Interleukin-1 Beta (IL-1β) is a potent pro-inflammatory cytokine produced primarily by activated macrophages, monocytes, dendritic cells, and microglia in mice (Mus musculus) in response to infection, tissue damage, or danger-associated molecular patterns. Synthesized as an inactive precursor (pro–IL-1β), it is cleaved into its active form by caspase-1 within inflammasome complexes—most notably the NLRP3 inflammasome—and signals through the IL-1 receptor type 1 (IL-1R1), activating NF-κB and MAPK pathways that promote fever, leukocyte recruitment, endothelial activation, and amplification of inflammatory responses. Murine IL-1β is central to widely used experimental models of sepsis, gout, rheumatoid arthritis, inflammatory bowel disease, neuroinflammation, metabolic disorders, and cancer, where dysregulated IL-1β production contributes to tissue injury and chronic inflammation. IL-1β–deficient, IL-1R1 knockout, and inflammasome-deficient mouse models have been instrumental in defining the molecular mechanisms of inflammasome activation and cytokine-driven pathology. As both a biomarker and therapeutic target, mouse IL-1β remains foundational in preclinical research investigating anti-inflammatory drugs, biologics targeting IL-1 signaling, and the broader role of innate immune activation in infectious and inflammatory diseases relevant to human health.