Tumor necrosis factor alpha and lymphotoxin alpha (TNF-α (for tumor necrosis factor alpha), LT-α (for lymphotoxin alpha; formerly known as TNF-β))

Tumor necrosis factor alpha (TNF-α) is a trimeric pro-inflammatory cytokine predominantly produced by macrophages, T cells, and natural killer cells; it exists in both membrane-bound and soluble forms and signals mainly via TNF receptors TNFR1 and TNFR2 to regulate inflammation, immune responses, cell death (apoptosis, necroptosis), and cell proliferation[2][3][6][7]. Dysregulation of TNF-α is implicated in the pathogenesis of multiple inflammatory and autoimmune diseases such as rheumatoid arthritis, Crohn’s disease, and psoriasis. Lymphotoxin alpha (LT-α; formerly TNF-β), encoded by a distinct gene (LTA), is structurally related, functions as a soluble homotrimer, and shares some receptor specificity and biological activities (particularly in the development of lymphoid organs and immune regulation), but with notable differences in tissue expression and function[5]. Drugs inhibiting TNF-α have transformed the treatment of autoimmune and inflammatory diseases, but carry risks related to immunosuppression. TNF-α and LT-α are archetypal representatives of the TNF superfamily, which play pleiotropic roles in inflammation, apoptosis, and tissue organization.

Other names

Tumor necrosis factor alpha: cachectin, TNF, TNFA, TNFαLymphotoxin alpha: Tumor necrosis factor beta, TNF-β, LT-α, lymphotoxin, TNFB

Neutralization of cytokine activity by direct binding; Inhibition of ligand-receptor interaction (blocking TNF-α or LT-α from activating TNFR1/TNFR2); Reduction of downstream pro-inflammatory signaling; Induction of apoptosis in pathological immune cells