TNF-alpha

Tumor necrosis factor (TNF, tumor necrosis factor alpha, TNFα, cachexin, or cachectin) is a cell signaling protein (cytokine) involved in systemic inflammation and is one of the cytokines that make up the acute phase reaction. It is produced chiefly by activated macrophages, although it can be produced by many other cell types such as CD4+ lymphocytes, NK cells, neutrophils, mast cells, eosinophils, and neurons.

84088-42-6
Roquinimex
84088-42-6
847871-99-2
847871-99-2
852391-15-2
852391-15-2
852391-19-6
Necrostatin 2
852391-19-6
852391-20-9
852391-20-9
SPD 304
869998-49-2

Background


An overview of TNF-alpha

Tumor necrosis factorα(TNF-α) is a kind of cytokine that can kill tumor cells directly without obvious toxicity to normal cells, and participates in normal inflammatory response and immune response. The human TNF-α precursor consists of 233 amino acids (26kDa) comprising a signaling peptide consisting of 76 amino acid residues. And under the action of TNF invertase (TACE), it can form a mature TNF-α (17kDa) with 157 amino acid residues by excising the signaling peptide. TNF-α has increased in many pathological states, including sepsis, malignancy, heart failure and chronic inflammatory disease. Increased tumor necrosis factor can also be found in the blood and joints of patients with severe rheumatoid arthritis.

Inhibition of TNF-alpha

Interferon (IFN) is a macromolecular TNF-α inhibitor, which is a monoclonal antibody. Its action mechanism is to bind directly with TNF-a, so as to prevent the combination of TNF-αand TNFR, and inhibit the transduction of its downstream signal transduction pathway, preventing the occurrence of inflammation. Or when the IFN and mTNF are combined, the cells can undergo reverse signal transduction, resulting in the effects of programmed cell death and cytokine inhibition by complement-dependent cytotoxic reaction or antibody dependent cell-mediated cytotoxicity (ADCC).

TNF-alpha and diseases

TNF-α is currently found to be the most antitumor activity of cytokines. In addition to its cytotoxic effect on tumor cells, TNF-α can also destroy vascular epithelium around solid tumors and, through thrombosis, block the blood supply of tumors, eventually leading to hemorrhagic necrosis, extinction, or disappearance of the tumor. TNF-α could inhibit the development of new blood vessels at a certain concentration. An TNF-α can obviously reduce the pressure of the interstitial tissue around the solid tumor, enlarge the gap of epithelium around the tumor, and change the permeability of the peripheral blood vessels, making the drugs of chemotherapy reach the target tissue.

References:

1. Huang, J., Zhou, Y., University, W., & De. (2015). Research progress on tumor necrosis factor α and its inhibitors. International Journal of Stomatology.