Tumor necrosis factor-alpha

Author: Prof. Dr. med. Peter Altmeyer

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Last updated on: 08.07.2022

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Cachectin; TNF; TNF-alpha; TNFSF2; TNFα; TNF-α; Tumor Necrosis Factor; Tumor necrosis factor alpha; Tumor necrosis factor ligand superfamily member 2; Tumor Necrosis Factor-α

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Multifunctional proinflammatory cytokine centrally involved in local and systemic inflammation. TNF-alpha is one of the best studied members of the so-called TNF/TNFR superfamily, a cytokine system that plays central roles in the immune response and in organogenesis, especially of the lymphatic system. Thus, it plays a central role in the pathogenesis of psoriasis as well as other inflammatory processes (Crohn's disease, arthritides; pathogenesis of contact allergy). It causes hemorrhagic necrosis in certain tumors.

General information
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TNF-α exists biologically in soluble or transmembrane-bound form. TNF-α molecules interact with at least 2 receptors (tumor necrosis factor receptor superfamily member 1A(TNFRSF1A) or tumor necrosis factor receptor superfamily member 1B (TNFRSF1B). The interaction of TNF-α with its receptors activates signaling cascades that can lead to apoptosis (via caspase-8; see caspases below) and cell activation (via NF-κB) (Note: NF-kappaB (nuclear factor-kappa B) is a fast-acting primary transcription factor present in all cell types. It is involved in cellular responses to stimuli such as cytokines and stress and plays a key role in regulating the immunological response to infection/ see also under transcription factors).

The balance of antagonistic effects of both signaling inductions depends on the cellular environment in which stimulation by TNF-α occurs. The NF-κB-mediated reaction is relevant for inflammation, in the course of which proinflammatory enzymes such as interleukins (especially IL-6 and IL-8) are released.

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TNF-α is mainly produced and released by macrophages, but also by a large number of other cells such as lymphocytes, mast cells, endothelial cells, cardiac muscle cells, fibroblasts as well as neuronal tissue. Large amounts of TNF-α are released in response to bacterial products (e.g. lipopolysaccharides) as well as interleukin-1β. Its formation is stimulated via Toll-like receptors and the MAP pathway as well as NF-kappaB. Furthermore, it has effects on lipid metabolism, blood coagulation, insulin resistance and various endothelial functions.

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TNF-α and its interactions with its receptors are pharmacologically important targets of various drugs. Drug classes which are effective in biological immunotherapy of various diseases, including Crohn's disease, rheumatoid arthritis and psoriasis. S.a. Infliximab, Etanercept, Golimumab.

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TNF-α was already described in 1975 as a factor that led to tumor regression in bacterial diseases.

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Last updated on: 08.07.2022