Description
Tumor necrosis factor-beta (TNF-β), also known as LT-α and TNFSF1, is a highly inducible, secreted protein and member of the TNF ligand superfamily. It mediates a large variety of inflammatory, immunostimulatory and antiviral responses (1). TNF-β is also involved in the formation of secondary lymphoid organs during development and plays a role in apoptosis (1). It forms heteromers with lymphotoxin-beta (LT-β) that anchor the complexes to the cell surface of activated T, B and LAK cells (2). TNF-β and TNF-α are structurally and functionally related proteins that bind to the same cell surface receptors (TNF RI and TNF RII) and produce a wide range of similar effects (3). TNF-β promotes the proliferation of fibroblasts and induces the synthesis of GM-CSF, G-CSF, IL-1, collagenase and prostaglandin E2 (4). In neutrophils, it induces the production of reactive oxygen species, increases phagocytosis and adhesion to the endothelium, as well as acting as a chemoattractant for these cells. TNF-β is a mitogen for B-lymphocytes while it inhibits the growth of osteoclasts and keratinocytes. It is cytoxic or cytostatic for many tumor cells (6). TNF-β has been implicated in the pathogenesis of several autoimmune diseases and it plays a significant role in the etiopathogenesis of multiple sclerosis (7). Genetic variations in this gene are associated with susceptibility to leprosy type 4 and psoriatic arthritis. TNF-β may also be involved in processes of wound healing