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Interleukin 1β (IL-1β) is a potent pro-inflammatory cytokine belonging to the interleukin 1 family. It is primarily produced by activated macrophages and plays a central role in mediating inflammatory responses and amplifying immune reactions. IL-1β exerts its effects by binding to the interleukin 1 receptor type I (IL-1RI), which is widely expressed on many cell types. This interaction triggers a cascade of inflammatory mediators, chemokines, and other cytokines that contribute to tissue damage and pain sensitization. While recombinant or purified forms of IL-1β have been used experimentally to stimulate bone marrow function, their clinical use has been limited due to significant toxicity such as fever, fatigue, hypotension, and systemic inflammation[2][6]. Instead, pharmacological strategies have focused on blocking IL-1 activity for treating autoinflammatory diseases like Cryopyrin-Associated Periodic Syndromes (CAPS), Familial Mediterranean Fever (FMF), Systemic Juvenile Idiopathic Arthritis (SJIA), rheumatoid arthritis, pericarditis, and other conditions where excessive IL-1 signaling drives pathology[2][3][8]. Approved anti–IL‑1 therapies include anakinra (recombinant human IL‑1Ra), rilonacept (soluble decoy receptor for both α/β isoforms), and canakinumab (monoclonal antibody against IL‑1β)[2][8].
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