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Interferon therapy is used (in combination with chemotherapy and radiation) as a treatment for some cancers. [45] This treatment can be used in hematological malignancy, such as in leukemia and lymphomas including hairy cell leukemia, chronic myeloid leukemia, nodular lymphoma, and cutaneous T-cell lymphoma. [45]
Interferon gamma (IFNG or IFN-γ) is a dimerized soluble cytokine that is the only member of the type II class of interferons. [5] The existence of this interferon, which early in its history was known as immune interferon, was described by E. F. Wheelock as a product of human leukocytes stimulated with phytohemagglutinin, and by others as a product of antigen-stimulated lymphocytes. [6]
3467 n/a Ensembl ENSG00000177047 n/a UniProt P05000 n/a RefSeq (mRNA) NM_002177 n/a RefSeq (protein) NP_002168 n/a Location (UCSC) Chr 9: 21.14 – 21.14 Mb n/a PubMed search n/a Wikidata View/Edit Human Interferon omega-1 is a protein that is encoded by the IFNW1 gene. Introduction Interferon omega-1 (IFN-ω) is a subtype of the Interferon type I family. The Interferon Type 1 family is made ...
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 ...
Interferon beta-1a (also interferon beta 1-alpha) is a cytokine in the interferon family used to treat multiple sclerosis (MS). [5] It is produced by mammalian cells, while interferon beta-1b is produced in modified E. coli. [6] Some research indicates that interferon injections may result in an 18–38% reduction in the rate of MS relapses. [7]
Interferon alfa-2b is an antiviral or antineoplastic drug. It is a recombinant form of the protein Interferon alpha-2 that was originally sequenced and produced recombinantly in E. coli [ 1 ] in the laboratory of Charles Weissmann at the University of Zurich , in 1980.
The receptor and interferon are taken inside the cell while bound to initiate expression of ISGs. [10] Interferon activation of ISGs uses the JAK-STAT signaling pathway to induce transcription of ISGs. ISGs can be divided based on what class of interferon they are activated by: type I, type II, or type III interferon. [1]
Research into the use of interferons to combat influenza began in the 1960s in the Soviet Union, culminating in a trial of 14,000 subjects at the height of the Hong Kong Flu of 1969, in which those treated prophylactically with interferon were more than 50% less likely to suffer symptoms, though evidence of latent infection was present. [7]