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Interferon & Receptor

Sino Biological offers a comprehensive set of tools for research on interferons and their receptors, including recombinant proteins, antibodies, ELISA kits, and ORF cDNA clones.

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    Interferon & Receptor Information

    Interferons belong to the large family of cytokines. Interferon is not a toxin designed to poison a key molecule in the cell. Instead, it is a message that is read by human cells. Interferon is one of a growing class of cytokines, proteins that deliver instructions from cell to cell. Normally, interferon, and the similar interleukins, mediate a continual conversation between cells about growth and defenses. Interferons are named after their ability to "interfere" with viral replication within host cells. Interferon was identified more than 50 years ago by Isaacs and Lindenmann during their studies of the phenomenon of viral interference, the ability of an active or inactivated virus to interfere with the growth of an unrelated virus. Today, more than 10 mammalian IFN species and numerous subspecies have been discovered, each with individual properties, but all having antiviral activity.

    Interferons are currently classified into three groups: type I, type II and type III IFNs. The type I IFNs include all IFNαs, IFNβ, IFNε, IFNκ, IFNω and IFNν. Humans have 12 different IFNαs and a single IFNβ. Type I IFN genes are clustered on the human chromosome 9. Each subtype is encoded by its own gene and regulated by its own promoter, and none of them contain introns. The different IFNαs and IFNβ differ substantially in their specific antiviral activities and in the ratios of antiviral to antiproliferative activities. However, the molecular basis of these differences is not yet known. All type I IFNs bind to the same interferon alpha/beta receptor (IFNAR) which consists of two major subunits: IFNAR1 and IFNAR2c (the βL subunit).

    Interferon alpha (IFN alpha) showed multiple effects on melanoma. Firstly, IFN alpha has the potential of promoting antigen presentation and re-polarizing the immune response toward Th1 response. Secondly, IFN alpha helps the recruitment of T cells and NK to tumor tissue and promotes the survival of memory T cells. Thirdly, IFN alpha could inhibit the angiogenesis of melanoma. Finally, IFN alpha might directly inhibit the proliferation of melanoma cells.

    Interferons are not only the first line of defence against viral infections such as hepatitis C virus infections, but they also have important roles during the chronic phase of viral infections. For over 20 years now, recombinant interferon alpha has been used for the treatment of chronic hepatitis C. The molecular mechanisms responsible for non-response to interferon are still not completely understood, but systematic analysis of liver biopsies revealed that the spontaneous activation of the endogenous interferon system in the liver of patients with chronic hepatitis C prevented response to interferon-based therapies. Moreover, recent genomewide association studies found a highly significant and strong association between genetic variants near the IFNλ3 gene, designated the IL28B genotype, with spontaneous clearance of hepatitis C virus as well as with response to treatment of chronic hepatitis C with pegylated interferon alpha and ribavirin.

    Interferon & Receptor References

    1. David S. Goodsell. (2001). The Molecular Perspective: Interferons. The Oncologist. 6(4): 374-375.
    2. Simone Mocellin, et al. (2010). Interferon Alpha Adjuvant Therapy in Patients With High-Risk Melanoma: A Systematic Review and Meta-analysis. J Natl Cancer Inst. 102(7): 493-501.
    3. Axel Hauschild MD, et al. (2008). Practical guidelines for the management of interferon-α-2b side effects in patients receiving adjuvant treatment for melanoma. Cancer. 112(5): 982-994.
    4. Ijaz S Jamall, et al. (2008). Is pegylated interferon superior to interferon, with ribavarin, in chronic hepatitis C genotypes 2/3? World J Gastroenterol. 14(43): 6627–6631.