ArticleFrontiers in immunology2019
Type I Interferon Receptor on NK Cells Negatively Regulates Interferon-γ Production.
Article in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 35 citations in OpenAlex.
- Enhancement of NK cell activity via DNA-sensing inhibition by Poxin transgene.Journal of advanced research · 2026Article
- From pathogenesis to therapeutic targeting: new insight into TAM receptors in rheumatoid arthritis.Cell & bioscience · 2025Review
- Type I interferon regulation of group I ILC subsets during both homeostasis and cytomegalovirus infection.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- A Type I IFN-Inducing Oncolytic Virus Improves NK Cell-Mediated Killing of Tumor Cells In Vitro Through Multiple Mechanisms.Viruses · 2025Article
- The effect of COVID-19 and sex differences on natural killer cell cytotoxicity.Frontiers in cellular and infection microbiology · 2025Article
- Targeting cGAS-STING: modulating the immune landscape of hepatic diseases.Frontiers in immunology · 2025Review
- Single cell transcriptomics shows that malaria promotes unique regulatory responses across multiple immune cell subsets.Nature communications · 2023Article
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- Natural killer cell-mediated contact dermatitis-like reaction induced by treatment with TLR3 ligand poly(I:C).Contact dermatitis · 2023Article
- Role of Innate Interferon Responses at the Ocular Surface in Herpes Simplex Virus-1-Induced Herpetic Stromal Keratitis.Pathogens (Basel, Switzerland) · 2023Review
- Integration of the Connectivity Map and Pathway Analysis to Predict Plant Extract's Medicinal Properties-The Study Case ofPlants (Basel, Switzerland) · 2022Article
- Type I interferon regulates proteolysis by macrophages to prevent immunopathology following viral infection.PLoS pathogens · 2022Article
- Human placental hematopoietic stem cell-derived natural killer cells (CYNK) recognize and eliminate influenza A virus-infected cells.Frontiers in immunology · 2022Article
- Early IFN-α signatures and persistent dysfunction are distinguishing features of NK cells in severe COVID-19.Immunity · 2021Article
- Review
- Review
- Immunoregulatory Functions of Interferons During Genital HSV-2 Infection.Frontiers in immunology · 2021Review
- Attenuating the Effects of Novel COVID-19 (SARS-CoV-2) Infection-Induced Cytokine Storm and the Implications.Journal of inflammation research · 2021Review
- Article
- Therapeutic Options for Coronavirus Disease 2019 (COVID-19) - Modulation of Type I Interferon Response as a Promising Strategy?Frontiers in public health · 2020Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
NK cells are a key antiviral component of the innate immune response to HSV-2, particularly through their production of IFN-γ. It is still commonly thought that type I IFN activates NK cell function; however, rather than requiring the type I IFN receptor themselves, we have previously found that type I IFN activates NK cells through an indirect mechanism involving inflammatory monocytes and IL-18. Here, we further show that direct action of type I IFN on NK cells, rather than inducing IFN-γ, negatively regulates its production during HSV-2 infection and cytokine stimulation. During infection, IFN-γ is rapidly induced from NK cells at day 2 post-infection and then immediately downregulated at day 3 post-infection. We found that this downregulation of IFN-γ release was not due to a loss of NK cells at day 3 post-infection, but negatively regulated through IFN signaling on NK cells. Absence of IFNAR on NK cells led to a significantly increased level of IFN-γ compared to WT NK cells after HSV-2 infection
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Registered trials
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.