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Tumor necrosis factor (TNF) is a pro-inflammatory cytokine that has the ability to destroy tumor cells (hence the name).
The tumor factors TNF-α and TNF-β are produced in macrophages and lymphocytes.
Tumor necrosis factor TNF binds to cell surface receptors. Binding of TNF-α to the receptor changes the conformation of the receptor structure, which leads to changes in the synthesis of proteins involved in cell proliferation, the development of an inflammatory response, and apoptosis (programmed cell death).
Serum TNF-α, as a systemic inflammatory marker, is associated with sepsis, trauma, and heart failure.
TNF-α has also been implicated in the pathogenesis of rheumatoid arthritis and inflammatory bowel disease. Therefore, TNF-α inhibitors (monoclonal antibodies) have been developed for the treatment of these conditions.
The TNF-α indicator is used to diagnose immune system diseases and monitor treatment outcomes.
Patient preparation – not necessary
study sample – Venous blood
Interpretation of results: Increased TNF-α levels are observed in sepsis, trauma, autoimmune and chronic inflammatory diseases (rheumatoid arthritis, ankylosing spondylitis, Crohn's disease, psoriasis), infectious diseases, and transplant rejection reactions.
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