IL1B encodes interleukin-1 beta, a potent pro-inflammatory cytokine essential for immune defense and the inflammatory response. The protein is initially produced as an inactive precursor and matured through inflammasome-mediated cleavage, particularly via the NLRP3 inflammasome 1. Mature IL-1β is released through gasdermin-D pores during pyroptosis, enabling its extracellular signaling. IL-1β orchestrates multiple facets of innate and adaptive immunity: it induces prostaglandin synthesis, neutrophil and T-cell activation, B-cell antibody production, and promotes Th17 differentiation. The cytokine synergizes with IL-12 to drive interferon-gamma production in Th1 cells and with TNF and IL-6 to promote angiogenesis through VEGF induction. In infection, IL-1β serves as a sensor of streptococcal pathogens, which activate it via the SpeB protease to trigger protective inflammatory responses. IL-1β dysregulation is implicated in diverse pathologies. In periodontitis, IL1B polymorphisms associate with disease susceptibility 2. Recent evidence suggests IL-1β elevation in acute urticaria may reflect reduced regulatory T cell function and contributes to disease pathogenesis 3. In multiple myeloma, IL-1β drives a neutrophil-stromal feed-forward loop that supports tumor growth and persists after treatment 4. IL-1β genetic variants influence psychosis risk through modulation of brain IL1B expression and structure 5. Multiple monoclonal antibodies and receptor antagonists targeting IL-1β—including canakinumab, gevokizumab, lutikizumab, and rilonacept—are approved or in development for autoinflammatory and autoimmune diseases, reflecting the therapeutic importance of controlling this cytokine.