IL-1

IL-1 is a core inflammatory cytokine family that links innate inflammation with acquired immunity and regulates host responses to infection, tissue injury, and sterile danger signals^[1]. Mechanistically, IL-1α and IL-1β signal through IL-1R1, recruit accessory receptor components, and activate inflammatory gene programs that amplify cytokines, chemokines, COX-2, iNOS, and matrix metalloproteinases^[2]. In disease models and human inflammatory disorders, deregulated IL-1α/IL-1β signaling contributes to severe acute or chronic inflammation, autoimmune disease, autoinflammatory disease, metabolic disease, neurological disease, degenerative disease, and cancer^[3]. Compared with related isoforms, IL-1α can act as an active precursor and is often cell-associated, whereas IL-1β requires enzymatic processing and functions mainly as a secreted inflammatory mediator^[2][3]. This isoform distinction matters in tumor models, where IL-1β promotes inflammation, tumor invasiveness, and immunosuppression, while cell-associated IL-1α can stimulate anti-tumor cell immunity^[2]. For experimental and translational research, IL-1 inhibitors provide pathway tools because anakinra, bermekimab, canakinumab, gevokizumab, and rilonacept have been evaluated across immune-mediated disorders^[4].- IL-1α and IL-1β share receptors but differ in localization, processing, and inflammatory context.- IL-1 blockade supports mechanistic studies of autoinflammation, tissue injury, tumor immunity, and cytokine amplification.