Tumor Necrosis Factor Alpha

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Tumor Necrosis Factor Alpha
Tumor Necrosis Factor Alpha

Video: Tumor Necrosis Factor Alpha

Video: Tumor Necrosis Factor Alpha
Video: Tumor necrosis factor-alpha (TNF-alpha) Mnemonic for USMLE 2024, November
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Tumor necrosis factor alpha

tumor necrosis alpha
tumor necrosis alpha

The term "tumor necrosis factor - alpha" appeared in 1975 (Kahektin). TNF or cachectin is a non-glycosylated protein that can have a cytotoxic effect on a tumor cell. The name of the protein TNF-alpha means its antitumor activity associated with hemorrhagic necrosis. It can cause hemorrhagic necrosis of some tumor cells, but does not damage healthy cells. It is formed by macrophages, eosinophils.

Tumor necrosis factor alpha is not detected in the blood serum of healthy people; its values increase in the presence of infection and bacterial endotoxins. With inflammation of bone tissue and other inflammatory processes, TNF-alpha is determined in the urine, affects tumor cells due to apoptosis, generation of reactive oxygen species and nitric oxide. Easily eliminates tumor cells and cells affected by the virus, participates in the development of the immune system's response to the introduction of an antigen, inhibits the formation of lymphocytes, has a radioprotective effect.

At low concentrations, TNF exhibits biological activity. Regulates the immune-inflammatory response in trauma or infections, is the main stimulant for neutrophils and endothelial cells, for their interaction and further movement of leukocytes, increasing the number of fibroblasts and endothelium during wound healing.

TNF-alpha can act as a hormone, entering the bloodstream, stimulates the formation of phagocytes, increases blood clotting, and reduces appetite.

In tuberculosis and cancer, it is an important factor in the development of cachexia. TNF plays an important role in the pathogenesis and choice of treatment for septic shock, rheumatoid arthritis, endometrial overgrowth, necrotic brain lesions, multiple sclerosis, pancreatitis, nerve damage, alcohol liver damage, diagnosis and prognosis during treatment of hepatitis C.

An increased level of TNF-alpha provokes chronic heart failure, exacerbation of bronchial asthma. The concentration of TNF increases in obesity, while clearly expressed in adipocytes of visceral adipose tissue, reduces the activity of the tyrosine kinase of the insulin receptor, delays the action of intracellular glucose transporters in muscle and adipose tissue.

It is also believed that the synthesis of endogenous TNF-alpha in some cases is a positive factor for patients, because it is a manifestation of protective forces. TNF is of great importance in detecting inflammatory processes in pregnant women. An increase in the expression of TNF in the amniotic fluid signals a violation of the intrauterine development of the fetus.

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The immune system of a newborn is determined by the level of TNF-alpha. The first stages of the study of TNF gave reason to think that it performs the function of providing antitumor protection in the body, but further studies have shown that it has a wide range of biological activity and takes part in physiological and pathological processes.

It is known that most of the cellular elements and biologically active substances are involved in the body's defense reactions and in the development of the inflammatory response. TNF has a pleiotropic effect and induces the expression of adhesive molecules on vascular endothelial cells, which act as a link between blood and tissues. Small doses of cachectin increase the body's resistance to, for example, malaria, while high doses promote infection and complicate the course of the disease until the death of a person.

An increased content of TNF in blood plasma was observed in patients suffering from acute and chronic gastritis, hepatitis, alcoholic and ulcerative colitis, as well as Crohn's disease (an unexplained granulomatous process affecting the gastrointestinal tract). Acute pancreatitis or pancreatic abscess, acute viral and bacterial manifestations in the respiratory tract are also accompanied by an increase in the level of monokine (TNF).

It is known that tobacco smoke activates macrophages and stimulates the production of cytokines. Therefore, in smokers, the biosynthesis and secretion of monokine by alveolar macrophages is 3 times higher than in healthy people. Excessive production of TNF is the cause of the development of depressive conditions and inflammatory skin diseases (systemic lupus erythematosus, pemphigus, psoriasis). A large role of cachectin in the development of acute and chronic nephritis, rheumatoid arthritis, inflammation and destruction of the vascular walls has been revealed.

It has been established that TNF is involved in the pathogenesis of diabetes mellitus, since when diagnosed, a significant concentration of it is determined in such patients. The amount of TNF is of great importance in the development of the "rejection syndrome" in patients with transplanted organs or tissues, the indices of TNF content in blood plasma serve as a criterion for clarifying the prognosis of conditions after transplantation.

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Article author: Mochalov Pavel Alexandrovich | d. m. n. therapist

Education: Moscow Medical Institute. IM Sechenov, specialty - "General Medicine" in 1991, in 1993 "Occupational Diseases", in 1996 "Therapy".

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