ArticleThe Journal of biological chemistry2018
Human interferon-ϵ and interferon-κ exhibit low potency and low affinity for cell-surface IFNAR and the poxvirus antagonist B18R.
Article in The Journal of biological chemistry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 33 citations in OpenAlex.
- Monkeypox virus replication and host response in vaginal and ectocervical epithelial cells.Virulence · 2026Article
- Age-dependent expression and antiviral activity of interferon epsilon in respiratory epithelium.Journal of virology · 2026Article
- Interferon Epsilon-Mediated Antiviral Activity Against Human Metapneumovirus and Respiratory Syncytial Virus.Vaccines · 2024Article
- A sensitive assay for measuring whole-blood responses to type I IFNs.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Convergent alterations in the tumor microenvironment of MYC-driven human and murine prostate cancer.Nature communications · 2024Article
- ARID4B loss leads to activated STAT1-dependent interferon pathway in mouse embryonic stem cells and during meso/endodermal differentiation.Journal of the Turkish German Gynecological Association · 2023Article
- Constitutive expression and distinct properties of IFN-epsilon protect the female reproductive tract from Zika virus infection.PLoS pathogens · 2023Article
- The Analyses of Cetacean Virus-Responsive Genes Reveal Evolutionary Marks in Mucosal Immunity-Associated Genes.Biochemical genetics · 2022Article
- Defining the characteristics of interferon-alpha-stimulated human genes: insight from expression data and machine learning.GigaScience · 2022Article
- Interferon Epsilon Signaling Confers Attenuated Zika Replication in Human Vaginal Epithelial Cells.Pathogens (Basel, Switzerland) · 2022Article
- Respiratory viral infections in otherwise healthy humans with inherited IRF7 deficiency.The Journal of experimental medicine · 2022Article
- Viral pathogen-induced mechanisms to antagonize mammalian interferon (IFN) signaling pathway.Cellular and molecular life sciences : CMLS · 2021Review
- The Role of Structure in the Biology of Interferon Signaling.Frontiers in immunology · 2020Review
- Context Is Key: Delineating the Unique Functions of IFNα and IFNβ in Disease.Frontiers in immunology · 2020Review
- Shared and Unique Features of Human Interferon-Beta and Interferon-Alpha Subtypes.Frontiers in immunology · 2020Review
- Porcine Interferon Complex and Co-Evolution with Increasing Viral Pressure after Domestication.Viruses · 2019Review
- Review
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
IFNϵ and IFNκ are interferons that induce microbial immunity at mucosal surfaces and in the skin. They are members of the type-I interferon (IFN) family, which consists of 16 different IFNs, that all signal through the common IFNAR1/IFNAR2 receptor complex. Although IFNϵ and IFNκ have unique expression and functional properties, their biophysical properties have not been extensively studied. In this report, we describe the expression, purification, and characterization of recombinant human IFNϵ and IFNκ. In cellular assays, IFNϵ and IFNκ exhibit ∼1000-fold lower potency than IFNα2 and IFNω. The reduced potency of IFNϵ and IFNκ are consistent with their weak affinity for the IFNAR2 receptor chain. Despite reduced IFNAR2-binding affinities, IFNϵ and IFNκ exhibit affinities for the IFNAR1 chain that are similar to other IFN subtypes. As observed for cellular IFNAR2 receptor, the poxvirus antagonist, B18R, also exhibits reduced affinity for IFNϵ and IFNκ, relative to the other IFNs. Taken together, our data suggest IFNϵ and IFNκ are specialized IFNs that have evolved to weakly bind to the IFNAR2 chain, which allows innate protection of the mucosa and skin and limits neutralization of IFNϵ and IFNκ biological activities by viral IFN antagonists.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.