Tumor necrosis factor

Serum glycoprotein produced by activated macrophages and other mammalian mononuclear leukocytes which has necrotizing activity against tumor cell lines and increases ability to reject tumor transplants. It mimics the action of endotoxin but differs from it. It has a molecular weight of less than 70,000 kDa.


Literally, tumor death factor. A cytokine (protein that helps regulate the immune system) that has shown potential to combat (kill) malignant (cancer) tumors. Tumor necrosis factor was discovered to be 1 0,000 times more toxic in humans than in rodents, where it had been tested for toxicity prior to human clinical tests. This example illustrates one potential pitfall of nontarget animal testing in that sometimes animal testing does not accurately reflect or foretell what will happen in humans. Another drawback to using TNF as a drug to combat human tumors is the fact that it is one of the substances released (in the disease rheumatoid arthritis) that destroys tissue in the joints. When released as part of the AIDS (disease), TNF causes cachexia, which is a “wasting away” of the body due to the body’s inability to process nutrients received via digestion.


A substance released by certain malignant tumors.


A polypeptide protein mediator or cytokine released primarily by macrophages and T lymphocytes; it helps regulate the metabolism of fats, the immune response, and some hematopoietic functions. There are two factors: alpha (TNFa), also called cachectin, produced by macrophages, and beta (TNF/3), called lymphotoxin, which is produced by activated CD4+ T cells. The functions of TNF are very similar to those of interleukin- 1. A monoclonal antibody against TNFa, infliximab, is used to treat rheumatoid arthritis and other diseases in which TNFa causes inflammatory damage. Antagonists to tumor necrosis factor (such as adalimumab, etanercept, and infliximab) are used to
treat diseases impacted by TNF, such as rheumatoid arthritis or Crohn disease.


 


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