IL1B encodes interleukin-1β, a potent pro-inflammatory cytokine 1 that functions as a key mediator of inflammatory responses essential for host defense against pathogens 2. Originally identified as the major endogenous pyrogen, IL1B induces prostaglandin synthesis, neutrophil and T-cell activation, B-cell antibody production, and fibroblast proliferation 3. The cytokine promotes Th17 differentiation and synergizes with IL-12 to induce interferon-γ synthesis in Th1 cells 1. Mechanistically, IL1B maturation depends on NLRP3 inflammasome activation 4, with the mature protein released extracellularly via gasdermin-D pores during pyroptosis 5. IL1B secretion occurs through non-conventional pathways dependent on stimulus strength 2. LPS-induced IL1B expression in macrophages requires metabolic reprogramming through pentose phosphate pathway, serine synthesis, and one-carbon metabolism to generate S-adenosylmethionine for histone methylation 6. Disease relevance spans inflammatory conditions and autoimmune diseases. IL1B dysregulation characterizes immune checkpoint inhibitor-induced arthritis, featuring IL1B-expressing myeloid cell expansion with enhanced NLRP3 activity 7. Elevated IL1B contributes to keratoconus susceptibility 8, and elevated trophoblast IL1B promotes miscarriage through suppressed cell migration and increased apoptosis 9. IL1B inhibition via D-mannose improves outcomes in endotoxemia and colitis models 10, offering therapeutic targets for inflammatory diseases.