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

Tumor necrosis factor alpha (TNF-α) is a pro-inflammatory cytokine mainly produced by macrophages, T cells, and natural killer cells and is a central mediator of inflammatory and immune responses[2][3][4]. TNF-α acts by binding to two primary receptors, TNFR1 and TNFR2, which are widely expressed and part of the larger TNF receptor superfamily[1][4]. TNF-β, also known as lymphotoxin alpha, is closely related and shares receptor usage but has distinct cellular sources and roles, being mainly produced by lymphocytes[1]. TNF-α and TNF-β trigger many downstream signaling pathways affecting cell survival, apoptosis, and the production of additional inflammatory mediators[2][3][4]. Both molecules are implicated in the pathogenesis of various autoimmune, inflammatory, oncologic, and infectious diseases[3][4]. Numerous highly effective biological drugs have been developed to inhibit TNF-α, and to a lesser extent TNF-β, in the treatment of inflammatory and autoimmune diseases such as rheumatoid arthritis, Crohn's disease, and psoriasis[3][4]. TNF inhibitors are associated with specific safety concerns, particularly immunosuppression and infection risk[3][4]. Note: This entry is marked **is_incorrect: true** because "TNF-α and TNF-β" refers to two related but distinct cytokines. They are often discussed together due to structural and functional similarities, but each is a unique therapeutic target with its own gene, expression pattern, and sometimes distinct roles[1][4]. For maximum precision, structured data should be separated into two entries: one for "Tumor necrosis factor alpha (TNF-α)" and one for "Tumor necrosis factor beta (lymphotoxin alpha/TNF-β)".

Other names

Tumor necrosis factor alpha (TNF-alpha)Tumor necrosis factor beta (TNF-beta)TNFCachectin (for TNF-α)Lymphotoxin alpha (for TNF-β)LTA (for lymphotoxin alpha/TNF-β)TNFATNFB

TNF inhibitor (competitive inhibition of TNF binding to receptors) Neutralization of TNF activity (antibody-mediated) Blockade of TNFR1/TNFR2 signaling Induction of apoptosis in TNF-producing cells (in some antibody drugs)