Tumor necrosis factors

Tumor necrosis factors (or the TNF-family) refers to a group of cytokines family that can cause cell death.

History

At the end of 19th century William Coley, a New York surgeon, described remission of tumours following bacterial infection. In 1975 a protein responsible for this process was identified and called tumor necrosis factor alpha (TNF-alpha)^[1].

An article on the history of fever therapy, as it was called, and TNF up to 1991, with references to clinical and double-blind studies but under the heading of complementary and alternative therapies, has been published^[2].

Mechanism

TNF acts via the TNF Receptor (TNF-R) and is part of the extrinsic pathway for triggering apoptosis. TNF-R is associated with procaspases through adapter proteins (FADD, TRADD, etc.) that can cleave other inactive procaspases and trigger the caspase cascade, irreversibly committing the cell to apoptosis.

TNF interacts with tumor cells to trigger cytolysis or cell death.

TNF interact with receptors on endothelial cells, which leads to increased vascular permeability allowing leukocytes access to the site of infection. This is a type of localized inflammatory response, although systemic release may lead to septic shock and death.

Types

• Tumor necrosis factor-alpha (TNF-α) is the most well-known member of this class, and sometimes referred to when the term "tumor necrosis factor" is used.

• Tumor necrosis factor-beta (TNF-β), also known as lymphotoxin is a cytokine that is induced by interleukin 10 ^[3]

References

External links

• MeSH Tumor+Necrosis+Factors

This protein-related article is a stub. You can help Wikipedia by expanding it.