Tumor necrosis factor

Tumor necrosis factor (TNF) is a signaling protein, or cytokine, that promotes inflammation and coordinates immune responses. Its effects depend on the receptor and cell context, ranging from cell survival to cell death.

TNF receptor 1: A widely expressed receptor that binds TNF and can activate inflammatory signaling or programmed cell death. It mediates many of TNF’s inflammatory and cell-death effects.
TNF inhibitors: Medicines that block TNF activity to reduce inflammation in autoimmune and inflammatory diseases. They directly counter TNF’s inflammatory signaling.
Septic shock: A life-threatening form of sepsis involving circulatory failure and dangerously low blood pressure. Excessive TNF and other inflammatory signals can contribute to shock during severe infection.
William B. Coley: An American surgeon who used bacterial preparations to provoke immune responses against tumors in the late nineteenth century. His experiments helped establish the idea that immune activation could affect tumors, a context behind TNF’s name.
Interleukin 1: A family of cytokines that promotes inflammation, fever, and immune activation. It overlaps with TNF in inflammatory effects but signals through different receptors.
TNF receptor 2: A TNF receptor found mainly on immune and endothelial cells that often supports cell survival and immune regulation. It provides a second route for TNF signaling, with effects distinct from TNF receptor 1.
Infliximab: A monoclonal antibody that binds TNF and is used to treat several inflammatory diseases. It is a widely used example of a drug that neutralizes TNF.
Cachexia: A wasting syndrome involving loss of muscle and fat that occurs in chronic disease. Persistent TNF signaling can contribute to appetite loss and tissue breakdown.
Lloyd J. Old: An American immunologist whose research helped establish tumor necrosis factor as a distinct cytokine. His group’s work helped identify and characterize TNF.
Interleukin 6: A cytokine involved in inflammation, immune regulation, and the acute-phase response. It can cooperate with TNF in inflammation, while having distinct signaling pathways and clinical targets.

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