Tumor necrosis factor-alpha, TNFα, is a human cytokine associated with systemic inflammation and is an integral component of the acute phase reaction. Primarily, activated macrophages produce TNFα, but other cell types such as natural killer cells, mast cells, T helper cells, eosinophils, and neutrophils can also produce TNFα. These cells produce TNFα as a stable 233 amino acid long homotrimer protein, from which a metalloprotease, TNFα-converting enzyme proteolytically cleaves and releases a soluble homotrimeric cytokine.
TNFα belongs to the TNF superfamily that comprises several transmembrane proteins. The human tumor necrosis factor alpha primarily regulates the immune cells. TNFα is an endogenous pyrogen and therefore, can induce fever, inflammation, and apoptotic cell death. TNFα can inhibit viral replication, oncogenesis, and along with interleukin (IL)-1 and IL-6 cells, it can also respond to sepsis.
When you browse for ‘What is Tumor Factor Necrosis Alpha’ online, you will get results for tumor necrosis factor (TNF), cachectin and cachexin.
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How do you define tumor necrosis factor? Tumor necrosis factor alpha or TNFα binds to two receptors, TNFR1 and TNFR2. Most tissues express the TNFR1 receptor, and both the soluble trimeric form and membrane-bound TNFα can activate the TNFR1 receptor. On the other hand, the immune system expresses the TNFR2 receptor, and the membrane-bound TNFα homotrimer activates the TNFR2 receptor. TNFα combined with IL-1 and IL-6 performs a broad spectrum of biological activity. TNFα can trigger the release of the corticotropin-releasing hormone and stimulate the hypothalamic-pituitary-adrenal axis. TNFα can stimulate the acute phase response in the liver and cause an increase in C-reactive protein levels. They can also promote serine-phosphorylation of IRS-q and induce insulin resistance.
TNFα is a potent neutrophil attractant. Tumor necrosis factor alpha function is to promote adhesion molecule expression and facilitate neutrophil migration. A local increase in TNF levels induces symptoms of inflammation. While high concentrations may induce shock-like symptoms, prolonged low TNF levels can cause cachexia.
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At NorthEast BioLabs, we use MSD, ELISA, and Luminex assays to detect tumor necrosis factor alpha (TNFα) in human plasma or serum. Following describes a Luminex protocol followed for the tumor necrosis factor alpha assay.
We begin with 200 μl of assay buffer in each well, shake it for 10 min at room temperature (RT), and decant it. Once we remove all the residues, we add 25 μl of the following components in appropriate wells: standard, control or samples, followed by assay buffer, serum matrix, and beads and are incubated overnight at 4 ℃. Once the beads capture an analyte, we add 50 μl of biotinylated detection antibody and incubate it for 1 hr at RT. We then incubate the wells with a 50 μl streptavidin-phycoerythrin, a reporter molecule to end the surface reaction. Last, we add 100 μl of the sheath or drive fluid and read the plate on a Luminex platform.
The assay is highly sensitive (0.3 pg/ml) with an intra-assay precision of < 10% and an inter-assay precision of < 20%. The assay is highly accurate with a 91% recovery in the serum matrix.
Tumor necrosis factor alpha or TNFα induces inflammatory responses in humans. The inflammatory responses activated are critical in several clinical conditions associated with autoimmune disorders. TNF inhibitors bind with greater affinity to TNFα and inhibit its tumor necrosis factor alpha function or activation. Some examples of TNF inhibitors are infliximab, adalimumab, certolizumab pegol, and etanercept. We should note that in some patients, TNF inhibitors might aggravate their disease condition or facilitate the onset of new autoimmunity.
Anti-TNF therapy has delivered average results for cancer treatment. Studies have shown that infliximab treatment in certain renal cell carcinoma patients caused prolonged stabilization of the disease. Similarly, etanercept treatment in breast and ovarian cancer patients showed prolonged stabilization of the disease via downregulation. On the other hand, studies combining infliximab or etanercept with gemcitabine for treatment of advanced pancreatic cancer could not show any efficacy in outcome when compared with the placebo group.
To learn more about the biological activity of TNFα and its detection assays, explore the resources below.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2631033/
https://www.webmd.com/rheumatoid-arthritis/how-does-tnf-cause-inflammation
https://www.sciencedirect.com/topics/medicine-and-dentistry/tumor-necrosis-factor
https://www.medicalnewstoday.com/articles/324841
https://www.sinobiological.com/resource/cytokines/what-is-tnf
Brain-Derived Neurotrophic Factor
Granulate Colony Stimulation Factor
Epidermal growth factor
Fas Ligand
Granulocyte Macrophage Colony Stimulating Factor
Leukemia Inhibitory Factor
Luteinizing hormone
Macrophage Migration Inhibitory Factor
Interferon Beta
Interferon Gamma
Transforming Growth Factor Beta 1
B Type Natriuretic Peptide
Glial Fibrillary Acidic Protein
Cystatin C
Hepatocyte Growth Factor
Interferon Alpha 2
Tumor Necrosis Factor Alpha
