Human Interleukin-1 Beta (IL-1β) is a potent pro-inflammatory cytokine produced primarily by activated macrophages, monocytes, and dendritic cells in response to infection, tissue injury, or danger-associated molecular patterns. Synthesized as an inactive precursor (pro–IL-1β), it is cleaved into its active form by caspase-1 within multiprotein inflammasome complexes—most notably the NLRP3 inflammasome—and subsequently signals through the IL-1 receptor type 1 (IL-1R1), activating NF-κB and MAPK pathways that drive fever, leukocyte recruitment, endothelial activation, and acute-phase protein production. IL-1β plays a central role in host defense against bacterial, viral, and fungal pathogens, but dysregulated or excessive IL-1β signaling contributes to a wide range of inflammatory and autoimmune conditions, including rheumatoid arthritis, gout, inflammatory bowel disease, type 2 diabetes, atherosclerosis, sepsis, and cytokine release syndromes. Elevated IL-1β is also implicated in neuroinflammatory disorders and certain cancers, where it can promote tumor progression and immune modulation. As both a biomarker and therapeutic target, IL-1β has been the focus of targeted biologic therapies such as IL-1 receptor antagonists and anti–IL-1β monoclonal antibodies. Consequently, human IL-1β is central to research on inflammasome biology, chronic inflammation, metabolic disease, and development of precision anti-inflammatory treatments.