Interleukin 1 beta (IL-1β) (IL-1β)

Interleukin 1 beta (IL-1β) is a potent pro-inflammatory cytokine that serves as a central mediator of the innate immune response and systemic inflammation (UniProt: P01584). It is produced primarily by activated macrophages as an inactive precursor, pro-IL-1β, which is cleaved into its mature, bioactive form by caspase-1 following the activation of the NLRP3 inflammasome (StatPearls: Interleukin 1). Once secreted, IL-1β binds to the Interleukin 1 receptor type 1 (IL-1R1), initiating a signaling cascade that induces the expression of other cytokines, chemokines, and adhesion molecules, and triggers physiological responses such as fever and pain (PMID: 31034446). Dysregulation of IL-1β is a primary driver in autoinflammatory conditions like Cryopyrin-Associated Periodic Syndromes (CAPS) and plays a significant role in chronic inflammatory diseases including gout, rheumatoid arthritis, and atherosclerosis (PMID: 28859337). Therapeutic targeting of IL-1β has proven effective through the use of monoclonal antibodies like canakinumab, which neutralizes the cytokine, and receptor antagonists like anakinra, which block its signaling (DrugBank). Recent clinical evidence, notably from the CANTOS trial, has also established IL-1β inhibition as a viable strategy for reducing cardiovascular risk in patients with a history of myocardial infarction and elevated inflammatory markers (NEJM: 10.1056/NEJMoa1707914).

Other names

IL-1 betaIL1BIL1F2CatabolinInterleukin-1 beta

Direct neutralization of the secreted cytokine by monoclonal antibodies, competitive inhibition of the IL-1 receptor by recombinant receptor antagonists, or sequestration of the cytokine by decoy receptors (traps) to prevent downstream pro-inflammatory signaling (DrugBank; PMID: 28859337).