Tumor necrosis factor-alpha; Lymphotoxin-alpha (TNF (for Tumor necrosis factor-alpha); LT-α (for Lymphotoxin-alpha))

Tumor necrosis factor-alpha and Lymphotoxin-alpha are **pro-inflammatory cytokines** of the TNF superfamily that play central roles in immune regulation, inflammation, apoptosis, and development of secondary lymphoid organs[1][2][5]. **TNF-α** is mainly produced by macrophages and other immune cells, acting as a potent mediator of systemic inflammation and a driver of cell death or survival depending on the cellular context[5]. **Lymphotoxin-alpha**, previously called TNF-beta, is produced by lymphocytes and is essential for the development and organization of secondary lymphoid organs such as lymph nodes, Peyer’s patches, and spleen[1][3]. Both function predominantly as soluble homotrimers (although LT-α can also form heterotrimers with LT-β), signal through TNF receptor family members, and are targets of biologic drugs (such as monoclonal antibodies and fusion proteins) for the treatment of autoimmune and inflammatory diseases[1][2][3][5].

Other names

TNFTNF-αCachectinLT-αTNF-βLTA

Neutralization of cytokine activity by binding to TNF-α or LT-α and preventing receptor interaction (monoclonal antibodies, fusion proteins) - Downregulation of downstream inflammatory signaling - Suppression of immune cell activation and cytokine production