Interferon-alpha 2 (IFN alpha-2) is one of 14 subtypes within the IFN-alpha class of Type I Interferons. The members of the IFN-alpha class, also known as alpha leukocyte interferons, encompass a group of distinct but closely related proteins which share approximately 80% amino acid (aa) sequence identity and have a similar globular structure composed of five alpha-helices. IFN-alpha class members signal through a common cell surface receptor complex composed of IFN-alpha R2 and IFN-alpha R1 subunits. As the first highly active IFN to be cloned and produced, IFN alpha-2 has become the prototypic IFN for academic and pharmaceutical research. The mature extracellular domain (ECD) of Mouse IFN alpha-2 shares 60% and 83% aa sequence identity with Human and rat, respectively. Murine IFN-alpha 2 can eliminate cardiac viral load and protect cardiomyocytes from injury in animals infected with coxsackievirus B3 (CVB3). IFN alpha-2 derived mutants with reduced IFNR2 binding inhibited HIV replication and mutants with more IFNAR1 binding potentiated antiviral activity.
IFNA1, also known as IFN-alpha and IFNA, belongs to the alpha/beta interferon family. Interferons(IFNs) are proteins made and released by host cells in response to the presence of pathogens such as viruses, bacteria, parasites, or tumor cells. They belong to the large class of glycoproteins known as cytokines. IFNs stimulate the production of two enzymes: a protein kinase and an oligoadenylate synthetase. They allow for communication between cells to trigger the protective defenses of the immune system that eradicate pathogens or tumors. IFNs can activate immune cells, such as natural killer cells and macrophages; they increase recognition of infection or tumor cells by up-regulating antigen presentation to T lymphocytes, and they also increase the ability of uninfected host cells to resist new infection by the virus. Leukocyte interferon is produced predominantly by B lymphocytes. Immune interferon is produced by mitogen- or antigen-stimulated T lymphocytes. IFNA1 is produced by macrophages and has antiviral activities.
Interferon-alpha/beta receptor alpha chain (IFNAR1) is a type I membrane protein that forms one of the two chains of a receptor for interferons alpha and beta. Binding and activation of the receptor stimulates Janus protein kinases, which in turn phosphorylate several proteins, including STAT1 and STAT2. The encoded protein also functions as an antiviral factor. Tyk2 slows down IFNAR1 degradation and that this is due, at least in part, to inhibition of IFNAR1 endocytosis. Mutant versions of IFNAR1, in which Tyr466 is changed to phenylalanine, can act in a dominant negative manner to inhibit phosphorylation of STAT2. These observations are consistent with a model in which IFNAR1 mediates the interaction between JAK kinases and the STAT transcription factors.
Component of the receptor for type I interferons, including interferons alpha, IFNB1 and IFNW1. Functions in general as heterodimer with IFNAR2 . Type I interferon binding activates the JAK-STAT signaling cascade, and triggers tyrosine phosphorylation of a number of proteins including JAKs, TYK2, STAT proteins and the IFNR alpha-and beta-subunits themselves. Can form an active IFNB1 receptor by itself and activate a signaling cascade that does not involve activation of the JAK-STAT pathway.
Interferons (IFNs) are natural glycoproteins belonging to the cytokine superfamily and are produced by the cells of the immune system of most vertebrates in response to challenges by foreign agents such as viruses, parasites, and tumor cells. Interferon-beta (IFN beta) is an extracellular protein mediator of host defense and homeostasis. IFN beta has well-established direct antiviral, antiproliferative, and immunomodulatory properties. Recombinant IFN beta is approved for the treatment of relapsing-remitting multiple sclerosis. The recombinant IFN beta protein has the theoretical potential to either treat or causes autoimmune neuromuscular disorders by altering the complicated and delicate balances within the immune system networks. It is the most widely prescribed disease-modifying therapy for multiple sclerosis (MS). Large-scale clinical trials have established the clinical efficacy of IFN beta in reducing relapses and slowing disease progression in relapsing-remitting MS. IFN beta therapy was shown to be comparably beneficial for opticospinal MS (OSMS) and conventional MS in Japanese. IFN beta is effective in reducing relapses in secondary progressive MS and may have a modest effect in slowing disability progression. In addition to the common antiviral activity, IFN beta also induces increased production of the p53 gene product which promotes apoptosis and thus has a therapeutic effect against certain cancers. The role of IFN-beta in bone metabolism could warrant its systematic evaluation as a potential adjunct to therapeutic regimens of osteolytic diseases. Furthermore, IFN beta might play a beneficial role in the development of chronic progressive CNS inflammation.
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