Tumor necrosis factor-alpha, a homotrimeric 17kD protein, is a potent mediator of inflammatory and metabolic functions. TNF-alpha was originally detected as a highly cytotoxic cytokine for tumor cells, it causes tumor necrosis in vivo and shows cytolytic activity against tumor cells in vitro. Further, TNF-alpha has been implied as central mediator in shock induced by gram negative micro-organisms. The cytokine TNF-alpha is found to be a central mediator in many inflammatory and immunological processes: it can be induced by various products of micro-organisms and by various cytokines. It also induces on its turn the production of many cytokines. Furthermore, TNF-alpha has also been found in inflammatory foci such as synovial effusions in rheumatoid arthritis, systemic circulation in septic shock, parasitemia and rejection of renal transplants. Signal transduction occurs via two types of TNF-receptors, the TNF-receptors 1 and 2. The receptors differ strongly in their intra-cellular signaling pathways. The TNF-alpha trimer interacts with either of the two types of TNF-R leading to receptor cross-linking.
Intended for research use only. Not for use in human, therapeutic, or diagnostic applications.