ArticlePloS one2014
Role of type I interferon receptor signaling on NK cell development and functions.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
22 citing papers in PubMed, 32 citations in OpenAlex.
- Type I interferon regulation of group I ILC subsets during both homeostasis and cytomegalovirus infection.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Granzyme B and melittin in cancer immunotherapy: molecular mechanisms and therapeutic perspectives in head and neck cancers.Frontiers in immunology · 2025Review
- Human Metapneumovirus-Induced Host microRNA Expression Impairs the Interferon Response in Macrophages and Epithelial Cells.Viruses · 2023Article
- Intact Type I Interferon Receptor Signaling Prevents Hepatocellular Necrosis but Not Encephalitis in a Dose-Dependent Manner in Rift Valley Fever Virus Infected Mice.International journal of molecular sciences · 2022Article
- Review
- Consequences of sex differences in Type I IFN responses for the regulation of antiviral immunity.Frontiers in immunology · 2022Review
- Loss of type I IFN responsiveness impairs natural killer cell antitumor activity in breast cancer.Cancer immunology, immunotherapy : CII · 2021Article
- A Role of Variance in Interferon Genes to Disease Severity in COVID-19 Patients.Frontiers in genetics · 2021Review
- Natural killer cells in inflammatory autoimmune diseases.Clinical & translational immunology · 2021Review
- NK cells: A double edge sword against SARS-CoV-2.Advances in biological regulation · 2020Review
- MYC functions as a switch for natural killer cell-mediated immune surveillance of lymphoid malignancies.Nature communications · 2020Article
- STAT1 Isoforms Differentially Regulate NK Cell Maturation and Anti-tumor Activity.Frontiers in immunology · 2020Article
- Tissue-resident cytotoxic innate lymphoid cells in tumor immunosurveillance.Seminars in immunology · 2019Review
- Non-redundant ISGF3 Components Promote NK Cell Survival in an Auto-regulatory Manner during Viral Infection.Cell reports · 2018Article
- Inflammatory monocytes require type I interferon receptor signaling to activate NK cells via IL-18 during a mucosal viral infection.The Journal of experimental medicine · 2017Article
- Chemical and Biological Properties of S-1-Propenyl-l-Cysteine in Aged Garlic Extract.Molecules (Basel, Switzerland) · 2017Review
- Type I Interferons and Natural Killer Cell Regulation in Cancer.Frontiers in immunology · 2017Review
- Interferon regulatory factor 2 protects mice from lethal viral neuroinvasion.The Journal of experimental medicine · 2016Article
- Type I IFN promotes NK cell expansion during viral infection by protecting NK cells against fratricide.The Journal of experimental medicine · 2016Article
- Type-I Interferon Responses: From Friend to Foe in the Battle against Chronic Viral Infection.Frontiers in immunology · 2016Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Type I interferons (IFN) are unique cytokines transcribed from intronless genes. They have been extensively studied because of their anti-viral functions. The anti-viral effects of type I IFN are mediated in part by natural killer (NK) cells. However, the exact contribution of type I IFN on NK cell development, maturation and activation has been somewhat difficult to assess. In this study, we used a variety of approaches to define the consequences of the lack of type I interferon receptor (IFNAR) signaling on NK cells. Using IFNAR deficient mice, we found that type I IFN affect NK cell development at the pre-pro NK stage. We also found that systemic absence of IFNAR signaling impacts NK cell maturation with a significant increase in the CD27+CD11b+ double positive (DP) compartment in all organs. However, there is tissue specificity, and only in liver and bone marrow is the maturation defect strictly dependent on cell intrinsic IFNAR signaling. Finally, using adoptive transfer and mixed bone marrow approaches, we also show that cell intrinsic IFNAR signaling is not required for NK cell IFN-γ production in the context of MCMV infection. Taken together, our studies provide novel insights on how type I IFN receptor signaling regulates NK cell development and functions.
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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.