Proinflammatory cytokine

An inflammatory cytokine or proinflammatory cytokine is a type of signaling molecule (a cytokine) that is excreted from immune cells like helper T cells (Th) and macrophages, and certain other cell types that promote inflammation. They 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) and play an important role in mediating the innate immune response. Inflammatory cytokines are predominantly produced by and involved in the upregulation of inflammatory reactions. An inflammatory cytokine or proinflammatory cytokine is a type of signaling molecule (a cytokine) that is excreted from immune cells like helper T cells (Th) and macrophages, and certain other cell types that promote inflammation. They 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) and play an important role in mediating the innate immune response. Inflammatory cytokines are predominantly produced by and involved in the upregulation of inflammatory reactions. Excessive chronic production of inflammatory cytokines contribute to inflammatory diseases, that have been linked to different diseases, such as atherosclerosis and cancer. Dysregulation has also been linked to depression and other neurological diseases. A balance between proinflammatory and anti-inflammatory cytokines is necessary to maintain health. Aging and exercise also play a role in the amount of inflammation from the release of proinflammatory cytokines. Therapies to treat inflammatory diseases include monoclonal antibodies that either neutralize inflammatory cytokines or their receptors. An inflammatory cytokine is a type of cytokine a (signaling molecule) that is secreted from immune cells and certain other cell types that promotes inflammation. Inflammatory cytokines are predominantly produced by T helper cells (Th) and macrophages and involved in the upregulation of inflammatory reactions. Therapies to treat inflammatory diseases include monoclonal antibodies that either neutralize inflammatory cytokines or their receptors. 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). Inflammatory cytokines play a role in initiating the inflammatory response and to regulate the host defence against pathogens mediating the innate immune response. Some inflammatory cytokines have additional roles such as acting as growth factors. Pro-inflammatory cytokines such as IL-1β, IL-6, and TNF-α also trigger pathological pain. 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.Excessive chronic production of inflammatory cytokines contribute to inflammatory diseases. that have been linked to different diseases, such as atherosclerosis and cancer. Dysregulation of proinflammatory cytokines have also been linked to depression and other neurological diseases. A balance between proinflammatory and anti-inflammatory cytokines is necessary to maintain health. Aging and exercise also play a role in the amount of inflammation from the release of proinflammatory cytokines. Due to its proinflammatory action, a proinflammatory cytokine tends to make the disease itself or the symptoms correlated to a disease worse by causing fever, inflammation, tissue destruction, and in some cases, even shock and death. Excessive amounts of proinflammatory cytokines have been shown to cause detrimental effects A proinflammatory cytokine affects functions of transporters and ion channels from the nephron. As a result, there is a change in the activity of the potassium ion (K+) channels that changes the transepithelial transport of solutes and water in the kidney. The kidney proximal tubule cells produce proinflammatory cytokines in response to lipopolysaccaride. Proinflammatory cytokines affect the renal K+ channels. IFNγ causes delayed suppression and acute stimulation of the 40 pS K+ channel. Also, transforming growth factor beta 1 (TGF-β1) activates the calcium-activated potassium channel (KCa3.1) which could be involved the detrimental effects of renal fibrosis. Graft-versus-host disease (GvHD) targets JAK 1 and 2, the human tyrosine kinase protein required for signaling in multiple cytokines. When these kinases are activated, signal proteins of the signal transducer and activator of transcription (STAT) protein family - which include transcription factors for target genes that serve proinflammatory roles - are phosphorylated. The severity of GvHD is highly variable and is influenced by the amount of native cells present in the environment along with other regulatory T cells, TH1, TH2, or TH17 phenotypes. Both CD4+ and CD8 IL-17 producing T cells have been shown to cause aTH1, causing tissue inflammation and resulting in severe GVHD.