Anagram & Information om | Engelska ordet IFNS

Exempel på hur man kan använda IFNS i en mening

• IFNs belong to the large class of proteins known as cytokines, molecules used for communication between cells to trigger the protective defenses of the immune system that help eradicate pathogens.
• The recognition of PAMPs by the PRRs triggers activation of several signaling cascades in the host immune cells like the stimulation of interferons (IFNs) or other cytokines.
• TAM receptor tyrosine kinases increase phagocytic clearance of apoptotic cells and inhibit immunological responses brought on by Toll-like receptors and type I interferons (IFNs) when they are activated by the ligands Gas6 and Protein S.
• Plasmacytoid dendritic cells (pDCs) are a rare type of immune cell that are known to secrete large quantities of type 1 interferon (IFNs) in response to a viral infection.
• Their classification as Interferons is due to their ability to induce an antiviral state, while their additional classification as cytokines is due to their chromosomal location as well as the fact that they are encoded by multiple exons, as opposed to a single exon, as most type-I IFNs are.
• Activation of various innate immune signaling pathways (TLR3, TLR4, TLR7, TLR8, TLR9, cGAS, RIG-I, MDA-5) leads to the rapid induction of type I IFNs due to their (mostly) intronless gene structure.
• IRF3 and IRF7 are themselves transcription factors that translocate into the nucleus and activate the transcription of type I IFNs genes and thereby initiate the process leading to the secretion of IFN by the infected cells.
• Recent studies demonstrated that miR-122 may directly regulate different aspects of the interferons (IFNs) signaling pathway to enhanced induction of anti-viral genes and inhibition of various virus.
• In Shu's lab they also showed that SIKE, a physiological suppressor of IKK epsilon and TBK1, can inhibit virus and TLR3-triggered IRF-3 activation; that RBCK1, a ubiquitin ligase, negatively regulates TNF and IL-1 triggered inflammatory signaling; that DAK, a dihydroacetone kinase, can inhibit MDA5; and that ISG56 (IFN-stimulated gene 56) is related to VSV replication, and negatively mediates virus-triggered induction of type I IFNs.
• Kagan's studies of the cGAS-STING pathway revealed mutant cGAS proteins that signal from within mitochondria to induce Type I IFNs, and the role of mitochondrial reactive oxygen species in potentiating inflammasome-mediated pyroptosis through oxidation of the pore forming protein gasdermin D.

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