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Tumor necrosis factors
From Wikipedia
Tumor necrosis factors (or the TNF-family) refers to a group of cytokines family that can cause cell death.
Contents |
History
At the end of 19th century William Coley, a New York surgeon, described remission of tumors 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 inhibited by interleukin 10 [3]
References
- ↑ Terlikowski SJ: Tumour necrosis factor and cancer treatment: a historical review and perspectives.
- ↑ Coley's Toxins
- ↑ Lippincott's Illustrated Reviews: Immunology. Paperback: 384 pages. Publisher: Lippincott Williams & Wilkins; (July 1, 2007). Language: English. ISBN 0781795435. ISBN 978-0781795432. Page 68
External links
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