Lymphotoxin-alpha (LTA) (LTA)

Lymphotoxin-alpha (LTA), historically known as Tumor Necrosis Factor-beta (TNF-beta), is a pro-inflammatory cytokine and a member of the tumor necrosis factor superfamily (UniProt: P01374). It is primarily secreted by activated lymphocytes and plays a crucial role in the development of secondary lymphoid organs and the regulation of immune responses (NCBI Gene: 4049). LTA exists as a soluble homotrimer (LTA3) that binds to TNF receptors 1 and 2, or as a membrane-bound heterotrimer with lymphotoxin-beta (LTA1-beta2) that signals through the lymphotoxin-beta receptor (LTBR) (PubMed: 12750173). Dysregulation of LTA signaling is implicated in the pathogenesis of various autoimmune diseases, including rheumatoid arthritis and multiple sclerosis, as well as in the progression of certain cancers and chronic inflammatory conditions (PubMed: 25654766). Therapeutic strategies targeting LTA include the use of decoy receptors like etanercept, which neutralizes both TNF-alpha and LTA, and investigational monoclonal antibodies like pateclizumab that specifically target LTA to reduce inflammation and tissue damage (DrugBank: DB00005).

Other names

Tumor necrosis factor-betaTNF-betaTumor necrosis factor ligand superfamily member 1TNFSF1LT-alpha

Neutralization of the soluble homotrimer or membrane-bound heterotrimer to prevent binding and signaling through TNFR1, TNFR2, or LTBR.