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Tumor necrosis factor (TNF), formerly known as TNF-α, is a chemical messenger produced by the immune system that induces inflammation. [5] TNF is produced primarily by activated macrophages , and induces inflammation by binding to its receptors on other cells. [ 6 ]
Peripheral immune cells are called to the site of injury via these cytokines and may now migrate across the compromised blood brain barrier into the brain. Common cytokines produced in response to brain injury include: interleukin-6 (IL-6), which is produced during astrogliosis, and interleukin-1 beta (IL-1β) and tumor necrosis factor alpha ...
The tumor necrosis factor (TNF) superfamily is a protein superfamily of type II transmembrane proteins containing TNF homology domain and forming trimers. Members of this superfamily can be released from the cell membrane by extracellular proteolytic cleavage and function as a cytokine .
While IL-1β is released by monocytes and macrophages, it is also present in nociceptive DRG neurons. IL-6 plays a role in neuronal reaction to an injury. TNF-α is a well known proinflammatory cytokine present in neurons and the glia. TNF-α is often involved in different signaling pathways to regulate apoptosis in the cells.
Lymphotoxin alpha, a member of the tumor necrosis factor superfamily, is a cytokine produced by lymphocytes. LT-α 1-β 2 can interact with receptors such as LT-β receptors. [12] Absence of LT-β on cell surfaces will diminish the ability of LT-α to form LT-α 1-β 2, thus decreasing its effective ability as a cytokine.
Lymphotoxin is a member of the tumor necrosis factor (TNF) superfamily of cytokines, whose members are responsible for regulating the growth and function of lymphocytes and are expressed by a wide variety of cells in the body.
The tumor necrosis factor receptor superfamily (TNFRSF) is a protein superfamily of cytokine receptors characterized by the ability to bind tumor necrosis factors (TNFs) via an extracellular cysteine-rich domain. [2] [3] With the exception of nerve growth factor (NGF), all TNFs are homologous to the archetypal TNF-alpha. [4]
ADAM17 is understood to be involved in the processing of tumor necrosis factor alpha at the surface of the cell, and from within the intracellular membranes of the trans-Golgi network. This process, which is also known as 'shedding', involves the cleavage and release of a soluble ectodomain from membrane-bound pro-proteins (such as pro-TNF-α ...