IL-1β (Interleukin-1 beta)

IL-1β (interleukin-1 beta) is a powerful pro-inflammatory cytokine. Your monocytes and macrophages make it. It drives acute inflammation. It also drives 'inflammaging', the low-grade, sterile inflammation that builds up with age. Switching it on takes two steps. First, a priming signal makes an inactive form, pro-IL-1β. (The signal is often a toll-like receptor sensing trouble.) Then a second signal assembles the NLRP3 inflammasome. That activates an enzyme, caspase-1. Caspase-1 snips pro-IL-1β into its active, secreted form. In aging tissue, senescent cells release IL-1β as part of the SASP. And falling SIRT2 activity lowers the bar for NLRP3 assembly. So the inflammation keeps going. Its causal role in artery disease was shown in CANTOS (Ridker et al., 2017; n=10,061). Canakinumab is an antibody that neutralizes IL-1β. The 150 mg dose cut major cardiovascular events by 15% versus placebo, independent of LDL. A pre-planned safety analysis even found dose-dependent drops in lung-cancer cases. Canakinumab is approved for autoinflammatory syndromes. But it is still experimental for heart disease. Colchicine blocks NLRP3 assembly a different way. It won regulatory approval for cardiovascular prevention in several countries by 2024.

Last reviewed: June 22, 2026

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