Tumor necrosis factor alpha and Interleukin-1 beta (TNF-α and IL-1β)

Tumor necrosis factor alpha (TNF-α) and Interleukin-1 beta (IL-1β) are central pro-inflammatory cytokines that regulate diverse aspects of the innate and adaptive immune responses, primarily by orchestrating and amplifying inflammation. TNF-α is secreted mainly by activated macrophages and can induce cellular responses ranging from apoptosis and cell survival to fever, by signaling through TNF receptors TNFR1 and TNFR2, thereby contributing to both host defense and the pathology of chronic inflammatory diseases[4]. IL-1β is predominantly produced by activated macrophages, monocytes, and dendritic cells following recognition of pathogens or cell injury, playing a major role in the induction of fever, leukocyte activation, differentiation of T helper cells (especially Th17), and acute-phase protein synthesis[6][7]. Both cytokines are established therapeutic targets in the treatment of autoimmune and chronic inflammatory diseases such as rheumatoid arthritis, Crohn’s disease, and others[4][6][7]. Therapeutic blockade of their activity has improved clinical outcomes but may increase susceptibility to infections and other immunologic complications.

Other names

Tumor necrosis factor alpha (TNF-α)TNFcachectinInterleukin-1 beta (IL-1β)IL1Bleukocytic pyrogenlymphocyte activating factor (historically)

TNF-α: Inhibitors block TNF-α binding to TNF receptors (TNFR1 and TNFR2), preventing downstream inflammatory signaling\nIL-1β: Inhibitors (anakinra is an IL-1 receptor antagonist; canakinumab/rilonacept target IL-1β directly) block receptor binding and subsequent pro-inflammatory signaling