Tumor necrosis factor

Tumor necrosis factor:
The TNF family, of which Tumor Necrosis Factor Alpha (TNF-A), is the prototype, contains more than 17 cytokines with important functions in adaptive and innate immunity.

Tumor Necrosis Factor Alpha (TNF-A):
·        TNF-A acts on endothelial cells and stimulates the expression of adhesion molecules and aids the extravasation of inflammatory cells.
·        It stimulates endothelial cells to express proteins that trigger blood clotting in the local small vessels, occluding them and cutting off blood flow.
·       This is important in preventing the pathogen from entering the bloodstream and spreading.
 ·      However, TNF-A can become catastrophic if the infection spreads. Sepsis causes a massive release of TNF-A from macrophages throughout the body. The systemic release of TNF-A into the bloodstream causes vasodilation, which leads to a loss of blood pressure and increased vascular permeability, leading to a loss of plasma volume and eventually to shock, known as septic shock.
Therapeutic uses of inhibition of TNF-A:
·        Anti-TNF-A antibodies have been found to induce remissions in rheumatoid arthritis and decrease inflammation in Crohn's disease.
·        There are two types of established drugs that are used to antagonize TNF-A in clinical practice:
·        The first type comprises the anti-TNF-A antibodies, such as infliximab and adalimumab, which bind to TNF-A and block its activity.
·        The second type I a recombinant human TNF receptor (TNFR) subunit p75-Fc fusion protein called etanercept, which binds TNF-A, thereby neutralizing its activity.

Tumor Necrosis Factor Beta (TNF-B):
·        It is secreted by Th1 cells and cytotoxic T cells, is also known as Lymphotoxin-alpha.
·        It activates macrophages and has a direct cytotoxic effect on some cells.
·        It also inhibits B cells.


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