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Interferons (IFNs, / ˌ ɪ n t ər ˈ f ɪər ɒ n / IN-tər-FEER-on [1]) are a group of signaling proteins [2] made and released by host cells in response to the presence of several viruses. In a typical scenario, a virus-infected cell will release interferons causing nearby cells to heighten their anti-viral defenses.
The type-I interferons (IFN) are cytokines which play essential roles in inflammation, immunoregulation, tumor cells recognition, and T-cell responses. In the human genome, a cluster of thirteen functional IFN genes is located at the 9p21.3 cytoband over approximately 400 kb including coding genes for IFNα (IFNA1, IFNA2, IFNA4, IFNA5, IFNA6, IFNA7, IFNA8, IFNA10, IFNA13, IFNA14, IFNA16 ...
Type III interferon receptors are expressed more specifically on epithelial cells and some immune cells such as neutrophils, and depending on the species, B cells and dendritic cells as well. [ 13 ] [ 14 ] [ 15 ] Therefore, their antiviral effects are most prominent in barriers, in gastrointestinal, respiratory and reproductive tracts.
Upon infection, STING from infected cells can sense the presence of nucleic acids from intracellular pathogens, and then induce interferon β and more than 10 forms of interferon α production. Type I interferon produced by infected cells can find and bind to Interferon-alpha/beta receptor of nearby cells to protect cells from local infection.
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Interferon-alpha, an interferon type I, was identified in 1957 as a protein that interfered with viral replication. [5] The activity of interferon-gamma (the sole member of the interferon type II class) was described in 1965; this was the first identified lymphocyte-derived mediator. [6]