IFN-ω is a type I interferon, which can be induced by virus-infected leukocytes. Members of the type I interferon family, which includes IFN-α, IFN-β, and IFN-ω, signal through IFNAR-1/IFNAR-2 receptor complex, and exert antiviral and antiproliferative activities. IFN-ω exhibits about 75% sequence homology with IFN- α, and contains two conserved disulfide bonds, which are necessary for full biological activity. Recombinant Human IFN-ω is a 19.9 kDa protein consisting of 173 amino acid residues.
Biochem/physiol Actions
IFN-ω is a type I interferon, which can be induced by virus-infected leukocytes. Members of the type I interferon family, which includes IFN-α, IFN-β, and IFN-ω, signal through IFNAR-1/IFNAR-2 receptor complex, and exert antiviral and antiproliferative activities. IFN-ω exhibits about 75% sequence homology with IFN- α, and contains two conserved disulfide bonds, which are necessary for full biological activity. Recombinant Human IFN-ω is a 19.9 kDa protein consisting of 173 amino acid residues.
Centrifuge the vial prior to opening. Reconstitute in water to a concentration of 1.0 mg/ml. Do not vortex. This solution can be stored at 2-8°C for up to 1 week. For extended storage, it is recommended to further dilute in a buffer containing a carrier protein (example 0.1% BSA) and store in working aliquots at -20°C to -80°C.
Host immunity to infection with SARS-CoV-2 is highly variable, dictating diverse clinical outcomes ranging from asymptomatic to severe disease and death. We previously reported reduced type I interferon in severe COVID-19 patients preceded clinical worsening. Further studies identified genetic mutations
Recent studies reported the presence of pre-existing autoantibodies (auto-Abs) neutralizing type I interferons (IFNs) in at least 15% of patients with critical or severe COVID-19 pneumonia. In one study, these auto-Abs were found in almost 20% of deceased patients across
Journal of clinical immunology, 42(3), 471-483 (2022-01-30)
Inborn errors of immunity (IEI) and autoantibodies to type I interferons (IFNs) underlie critical COVID-19 pneumonia in at least 15% of the patients, while the causes of multisystem inflammatory syndrome in children (MIS-C) remain elusive. To detect causal genetic variants
Circulating autoantibodies (auto-Abs) neutralizing high concentrations (10 ng/mL, in plasma diluted 1 to 10) of IFN-α and/or -ω are found in about 10% of patients with critical COVID-19 pneumonia, but not in subjects with asymptomatic infections. We detect auto-Abs neutralizing
Coronavirus disease 2019 (COVID-19) exhibits a wide spectrum of clinical manifestations, ranging from asymptomatic to critical conditions. Understanding the mechanism underlying life-threatening COVID-19 is instrumental for disease prevention and treatment in individuals with a high risk. We aimed to identify
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