Tumor necrosis factor-alpha (TNFa) in humans is a pleiotropic inflammatory cytokine. It is expressed by many different stimulated cell types including monocytes, endothelial cells, fibroblasts and both T and B-lymphocytes, but especially by macrophages. It affects most organs. The production of TNF alpha is induced by IL-1, PDGF, IFN-beta, NGF, Oncostatin M and certain fungal, viral, and parasitic invasions. Bacterial lipopolysaccharide is an especially potent stimulus.
The primary role of TNFa is in the regulation of immune cells. TNF a mediates septic shock in response to infection. It initiates a cascade of cytokines and increases vascular permeability, thereby recruiting macrophages and neutrophils. TNFa secreted by macrophages causes blood clotting which helps contain infection. TNFa is also able to induce apoptotic cell death or inflammation, and to inhibit viral replication. It possesses growth stimulating, inhibitory, and self regulatory properties. Dysregulation of TNFa production has been implicated in a variety of human diseases, as well as cancer.
The presence of TNFa is responsible for diverse immunomodulatory and toxic effects. For instance, TNFa induces neutrophil proliferation during inflammation, but it also induces neutrophil apoptosis upon binding to the TNF-R55 receptor. TNFa causes necrosis of some types of tumors, but promotes growth of other types. Low levels may aid in maintaining homeostasis by regulating the body's circadian rhythm, and may promote remodeling or replacement of injured and senescent tissue by stimulating fibroblast growth. High levels of TNFa correlate with increased risk of mortality.
TNF-A, TNF-a, TNF alpha, cachexin , cachectin; tumor necrosis factor-alpha, TNFSF2, TNFSF1A.
This protein-A purified antibody was prepared from whole rabbit serum produced by repeated immunizations with a recombinant protein raised in yeast, corresponding to 154 amino acids of mature swine TNFa.