Tumor necrosis factor
Encyclopedia : T : TU : TUM : Tumor necrosis factor
Tumor necrosis factor alpha drawn from PDB [1TNF ].
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| bgcolor="#eeeeee" | [TNF ] TNFA
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| bgcolor="#e7dcc3" | Entrez
| bgcolor="#eeeeee" | [7124 ]
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| bgcolor="#e7dcc3" | OMIM
| bgcolor="#eeeeee" | [191160 ]
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| bgcolor="#e7dcc3" | RefSeq
| bgcolor="#eeeeee" | [NM_000594 ]
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| bgcolor="#e7dcc3" | UniProt
| bgcolor="#eeeeee" | [P01375 ]
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| bgcolor="#e7dcc3" | PDB
| bgcolor="#eeeeee" | [Other data
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| bgcolor="#eeeeee" | [Locus
| bgcolor="#eeeeee" | Chr. 6 [p21.3 ]
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In medicine , tumor necrosis factor alpha (TNFα, cachexin or cachectin) is an important cytokine involved in systemic inflammation and the acute phase response .
History and nomenclature
TNFα was isolated in 1975 by Carswell et al as a soluble factor released by host cells that caused necrosis of a transplanted tumor , "sarcoma Meth A". Although TNFα does cause the necrosis of some tumors, it may stimulate the growth of others. In that sense, the name is somewhat of a misnomer .
Structure
TNFα is a member of a group of other cytokine s that all stimulate the acute phase reaction . It is a 185 amino acid glycoprotein peptide hormone , cleaved from a 212 amino acid-long propeptide on the surface of macrophage s. Some cells secrete shorter or longer isoforms. Genetically it maps to chromosome 6p21.3 in humans.
Physiology
TNFα is released by white blood cell s, endothelium and several other tissues in the course of damage, e.g. by infection . Its release is stimulated by several other mediators, such as interleukin 1 and bacterial endotoxin . It has a number of actions on various organ systems, generally together with interleukin s 1 and 6:
A locally increasing concentration of TNFα will cause the cardinal signs of Inflammation to occur: Heat, swelling, redness and pain.
Pharmacology
Inhibition of TNFα with a monoclonal antibody , such as infliximab (Remicade®) or adalimumab (Humira®); or a circulating receptor fusion protein such as etanercept (Enbrel®), are used in modern treatment of various autoimmune disorder s such as rheumatoid arthritis , ankylosing spondylitis , Crohn's disease and psoriasis . Clinical trials regarding the effectiveness of these drugs on hidradenitis suppurativa are currently ongoing. A fourth anti-TNF biologic, certolizumab pegol, is expected to receive approval for human use in the near future.
Such drugs may raise the risk of contracting tuberculosis or causing a latent infection to become active. The anti-TNF monoclonal antibody biologics, Infliximab and adalimumab, which are both currently FDA approved for human use, have label warnings which state that patients should be evaluated for latent TB infection and treatment should be initiated prior to starting therapy with these medications.
TNF or the effects of TNF are also inhibited by a number of natural compounds, including curcumin (an ingredient in turmeric ) and catechin s (in green tea )[[Citing sources citation needed ]] .
Reference
Carswell EA, Old LJ, Kassel RL, Green S, Fiore N, Williamson B. An endotoxin-induced serum factor that causes necrosis of tumors. Proc Natl Acad Sci U S A 1975;72:3666-70. PMID 1103152. See also
External link
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