TNK2

From WikiMD's Wellness Encyclopedia


Introduction[edit | edit source]

Tumor Necrosis Factor alpha (TNFα) is a cytokine involved in systemic inflammation and is part of the body's immune response. It is a member of a group of cytokines that stimulate the acute phase reaction. TNFα is produced chiefly by activated macrophages, although it can be produced by many other cell types such as lymphocytes, natural killer cells, and neurons.

Structure and Function[edit | edit source]

TNFα is a 17 kDa protein that forms a homotrimer in its active form. It is encoded by the TNF gene located on chromosome 6 in humans. TNFα is a potent pro-inflammatory cytokine and has a wide range of actions in the immune system, including:

  • Inducing fever by acting as an endogenous pyrogen.
  • Inducing apoptotic cell death.
  • Inhibiting tumorigenesis and viral replication.
  • Inducing cachexia, a wasting syndrome often seen in chronic disease.
  • Stimulating the acute phase response in the liver.

Mechanism of Action[edit | edit source]

TNFα exerts its effects by binding to its receptors, TNFR1 and TNFR2, which are present on the surface of many cell types. The binding of TNFα to these receptors triggers a cascade of intracellular signaling pathways, including the activation of NF-κB, a transcription factor that regulates the expression of genes involved in inflammation, immunity, and cell survival.

Clinical Significance[edit | edit source]

TNFα plays a critical role in the pathogenesis of several inflammatory diseases, including:

Due to its role in these diseases, TNFα is a target for therapeutic intervention. TNF inhibitors, such as infliximab, etanercept, and adalimumab, are used to treat these conditions by blocking the action of TNFα.

Research and Developments[edit | edit source]

Ongoing research is focused on understanding the complex role of TNFα in various diseases and developing new therapeutic strategies to modulate its activity. Studies are also exploring the role of TNFα in cancer, where it can have both tumor-promoting and tumor-suppressing effects depending on the context.

Also see[edit | edit source]




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Contributors: Prab R. Tumpati, MD