Interferon-alpha 2 (IFN alpha-2) is one of 14 subtypes with anin 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 an human and rat, respectively. Murine IFN-alpha 2 can eliminate cardiac viral load and protect cardiomyocytes from injury in animals infected with an coxsackievirus B3 (CVB3). IFN alpha-2 derived mutants with an reduced IFNR2 binding inhibited HIV replication and mutants with an more IFNAR1 binding potentiated antiviral activity.
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.
Interleukin-29 (IL-29) is a secreted protein which belongs to the IL-28/IL-29 family. IL-29 is a cytokine with immunomodulatory activity. IL-29 is highly similar in amino acid sequence to the IL-28. IL-28 and IL-29 are induced by viral infection and showed antiviral activity. IL-28 and IL-29 interacted with a heterodimeric class II cytokine receptor that consisted of IL-10 receptor beta (IL-10R beta) and an orphan class II receptor chain, designated IL-28R alpha. IL-29 plays an important role in host defenses against microbes and its gene is highly upregulated in cells infected with viruses. IL-29 may play a role in antiviral immunity. IL-29 up-regulates MHC class I antigen expression. It is a Ligand for the heterodimeric class II cytokine receptor composed of IL10RB and IL28RA. The ligand/receptor complex seems to signal through the Jak-STAT pathway.
Interleukin-28B; also known as Cytokine Zcyto22; Interferon lambda-3; Interferon lambda-4; IFNL3; IFNL4; ZCYTO22 and IL28B; is a secreted cytokine which belongs to the IL-28/IL-29 family. IL-28 has also been shown to play a role in the adaptive immune response. IL28B has immunomodulatory activity and up-regulates MHC class I antigen expression. IL28B displays potent antiviral activity and antitumor activity. In addition; IL28B is a ligand for the heterodimeric class II cytokine receptor composed of IL10RB and IL28RA. The ligand/receptor complex seems to signal through the Jak-STAT pathway.
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