Tumor necrosis factor alpha(TNF-alpha)

Proinflammatory cytokine.

Considered as an inflammatory cytokine involved in various immune responses.

Promotes the inflammatory response, which, in turn, drives autoimmune disorders.

TNF-alpha represents a common effective pathway that acts down stream in the inflammatory process.

TNFN alpha functionally is an important activator and product of macrophages that stimulate cytokine production in immune cells and activates fibroblasts, with resulting tissue remodeling.

Tumor necrosis factor-alpha (TNF-alpha) is an inflammatory cytokine produced upon acute inflammation and is an important signaling molecule responsible for inducing apoptosis or necrosis.

TNF-alpha exerts its effects by binding to various membrane receptors that belong to the TNF Receptor superfamily. 

With age, TNF-alpha serum levels negatively correlate with T cell function.

Additionally, elevated TNF-alpha levels are associated with increased systemic inflammation and contribute to inflammatory diseases like rheumatoid arthritis.

TNF-alpha signaling is thought to be up-regulated during inflammaging and contributes to cellular senescence and immune exhaustion.

TNF-alpha is also produced by neutrophils and activated T cells, which are enriched in the inflamed synovial membrane and entheseal structures with inserted tendons and ligaments in arthritis and in the intestinal wall in inflammatory bowel disease.

TNFN alpha is a stimulator of osteoclasts and accounts for osteoporosis seen in IMIDs, as well as formation of bone erosion in rheumatoid arthritis and psoriatic arthritis.

Promotes inflammation and is a t high levels when systemic inflammation and catabolic conditions exist.

Composed of three identical protein chains that brings three copies of TNF receptors together and initiates a cascade of signaling interactions inside a target cell.

2 active forms, one bound to the cell membrane which is released by a membrane-bound metalloproteinase to a second soluble form.

Virtually all cells display TNF receptors on their surfaces.

Its receptors p55 and p75 are expressed in a variety of cells.

p55 is noninducible an inducible at the transcriptional level by external stimuli.

Associated with fatigue, sleepiness, fever, pain, cognitive impairment, anorexia and depression.

Tumor necrosis factor alpha(TNF-α)-plays a major role modulating many inflammatory and immunologic disease.

It is directly toxic to the pancreatic beta cells, which ja been shown to promote the development of immune diabetes in animal models.

Signaling can be used for defense against infection.

Can direct a virus infected cell to destroy itself by apoptosis and in the presence of lipopolysaccharide on bacterial surfaces stimulates blood cells to release TNF promoting an inflammation to fight infection.

Signaling promotes remodeling of tissues such that TNF on blood cell surfaces promotes proliferation of lymphocytes in some instances and in on other occasions forces cells into apoptosis.

Can lead to inflammatory states, sepsis and arthritis.

It may have adverse effects in patients with heart failure and reduced ejection fraction.
Golimumab is a human IgG  Kappa monoclonal antibody specific for TNF-alpha  Alpha it is approved for autoimmune diseases such as rheumatoid arthritis, ulcerative colitis, polly articular juvenile idiopathic arthritis, and axial  spondyloarthritis and chill children two years of age or older.

Tumor necrosis factor alpha is efficacious in all major forms of arthritis as well as the two main forms of inflammatory bowel disease.

Giant cell arteritis does not respond to TNF alpha inhibition, and multiple sclerosis may even worsen with TNF-alpha inhibitors.


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