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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 ]
Therapies to treat inflammatory diseases include monoclonal antibodies that either neutralize inflammatory cytokines or their receptors. [2] Inflammatory cytokines include interleukin-1 (IL-1), IL-12, and IL-18, tumor necrosis factor alpha (TNF-α), interferon gamma (IFNγ), and granulocyte-macrophage colony stimulating factor (GM-CSF). [3]
A TNF inhibitor is a pharmaceutical drug that suppresses the physiologic response to tumor necrosis factor (TNF), which is part of the inflammatory response.TNF is involved in autoimmune and immune-mediated disorders such as rheumatoid arthritis, ankylosing spondylitis, inflammatory bowel disease, psoriasis, hidradenitis suppurativa and refractory asthma, so TNF inhibitors may be used in their ...
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.
The signaling of the LT-β receptor may induce the inflammatory properties of specific cancerous cell lines, and that the elimination of LT-β receptors may hinder tumor growth and lower inflammation. [4] [11] [13] Mutations in the regulatory factors involved in lymphotoxin signaling may increase the risk of cancer development. [13]
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. [26] TNF-alpha exerts its effects by binding to various membrane receptors that belong to the TNF Receptor superfamily.