Tumor necrosis factor (covers both alpha and beta forms) (TNF (includes TNF-α and TNF-β; TNF-α and TNF-β are respective abbreviations))

Tumor necrosis factor refers to a group of closely related cytokines, principally tumor necrosis factor alpha (TNF-α) and tumor necrosis factor beta (TNF-β, also called lymphotoxin-alpha). Both are important immune signaling proteins involved in the regulation of inflammation, immune responses, and cell death. TNF-α is a trimeric cytokine produced primarily by macrophages and plays a central role in mediating acute and chronic inflammation. It is initially synthesized as a membrane-bound precursor that is cleaved to release a soluble active form. TNF-β is produced mainly by lymphocytes and shares many structural and receptor interactions with TNF-α, but has some distinct biological activities. Both signals are primarily transmitted through the tumor necrosis factor receptor superfamily (especially TNFR1 and TNFR2), leading to diverse outcomes including apoptosis, necroptosis, and cell survival. Excess TNF activity is a major driver of autoimmune and autoinflammatory diseases, making these molecules important therapeutic targets for biologic agents designed to block their function[1][2][3][4][5][7].

Other names

Tumor necrosis factor alpha (TNF-α)Tumor necrosis factor beta (TNF-β)Lymphotoxin-alpha (for TNF-β)Cachectin (for TNF-α)

TNF inhibition (blockade of TNF binding to its receptor; neutralizing antibody or decoy receptor action); Antagonism of TNF receptor activation; Induction of immune cell apoptosis via reverse signaling (some cases)