Background |
Tumor Necrosis Factor-alpha (TNF-alpha) is a multifunctional pro-inflammatory cytokine, mainly secreted by activated macrophages. TNF-alpha was named for its remarkable ability to cause hemorrhagic necrosis to tumors in mice. It is implicated with a variety of biological procedures including systemic inflammation, cell proliferation, apoptosis, lipid metabolism, and coagulation. The pleiotropic attribute of TNF-alpha regulation is associated with its ability to trigger multiple signalling pathways simultaneously. It is well documented that TNF-alpha functions through its receptors, TNFR1 (p55) and TNFR2 (p75). TNF-alpha not only contributes to the immune response to bacterial, fungal, viral and parasitic invasions, but also functions in tissue remodeling, autoimmune-diseases and the necrosis of specific tumors. TNF-alpha hyper-expression in response to some bacterial components such as LPS can cause life threatening septic shock. Recombinant TNF-alpha, in combination with chemotherapy, has been applied for treatment of soft sarcomas, melanomas and other irresectable tumors. Anti-TNF-alpha therapy has been used for treatment of rheumatoid arthritis. |