ArticleThe Journal of experimental medicine2016
Type I IFN promotes NK cell expansion during viral infection by protecting NK cells against fratricide.
Article in The Journal of experimental medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 140 papers.
What it found
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Who cites it
140 citing papers in PubMed, 210 citations in OpenAlex.
- Different Innate and Adaptive Immune Responses to SARS-CoV-2 Infection of Asymptomatic, Mild, and Severe Cases.Frontiers in immunology · 2020Trial
- Interferon Alpha Induces Sustained Changes in NK Cell Responsiveness to Hepatitis B Viral Load Suppression In Vivo.PLoS pathogens · 2016Trial
- Type I IFN coordinates resistance and tolerance against Zika virus disease by inducing NK cell recruitment and limiting neutrophil-driven neuropathology in the brain.Brain, behavior, & immunity - health · 2026Article
- Beyond oncogenesis: the unexplored benefits of viruses in cancer immunity.Nature reviews. Cancer · 2026Review
- Therapeutic bacteria-trained NK cells confer long-term protection against cancer metastasis.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- Implications of RNA virus persistence for post-acute sequelae and chronic inflammatory syndromes.Nature immunology · 2026Review
- Stepwise epigenetic signal integration drives adaptive programming of cytotoxic lymphocytes.Immunity · 2026Article
- Macrophages From Latently Infected Mice Have Trained Immunity to HSV-1.Investigative ophthalmology & visual science · 2026Article
- The cGAS-STING pathway in fibroblast microenvironment: from molecular mechanisms to targeted therapies.Apoptosis : an international journal on programmed cell death · 2026Review
- Interferon-α enhances NK cell function to counteract autologous platelet-mediated tumor immune evasion.Cancer cell international · 2026Article
- The TRIM3/TLR3 axis overrides IFN-β feedback inhibition to suppress NSCLC progression.Cell death & disease · 2026Article
- Delayed type I interferon response and the subsequent out-of-sequence cytokine signal inhibit T cell induction in non-surviving Ebola virus-infected patients.Frontiers in immunology · 2026Article
- TCF19 drives a broad transcriptional program that potentiates optimal innate and adaptive functions of antiviral NK cells.Nature immunology · 2025Article
- Quantitation of TAK-981 in human plasma via LC-MS/MS and its application in clinical trials.Bioanalysis · 2025Article
- Review
- Protein-S-nitrosylation of human cytomegalovirus pp65 reduces its ability to undermine cGAS.Journal of virology · 2025Article
- Nerve- and airway-associated interstitial macrophages mitigate SARS-CoV-2 pathogenesis via type I interferon signaling.Immunity · 2025Article
- Splenic TNF-α signaling potentiates the innate-to-adaptive transition of antiviral NK cells.Immunity · 2025Article
- JAK inhibitor withdrawal causes a transient pro-inflammatory cascade: A potential mechanism for major adverse cardiac events.PloS one · 2025Article
- Role and mechanism of gut microbiota in regulating interferon-mediated programmed cell death in colorectal cancer.Frontiers in immunology · 2025Review
80 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Type I interferon (IFN) is crucial in host antiviral defense. Previous studies have described the pleiotropic role of type I IFNs on innate and adaptive immune cells during viral infection. Here, we demonstrate that natural killer (NK) cells from mice lacking the type I IFN-α receptor (Ifnar(-/-)) or STAT1 (which signals downstream of IFNAR) are defective in expansion and memory cell formation after mouse cytomegalovirus (MCMV) infection. Despite comparable proliferation, Ifnar(-/-) NK cells showed diminished protection against MCMV infection and exhibited more apoptosis compared with wild-type NK cells. Furthermore, we show that Ifnar(-/-) NK cells express increased levels of NK group 2 member D (NKG2D) ligands during viral infection and are susceptible to NK cell-mediated fratricide in a perforin- and NKG2D-dependent manner. Adoptive transfer of Ifnar(-/-) NK cells into NK cell-deficient mice reverses the defect in survival and expansion. Our study reveals a novel type I IFN-dependent mechanism by which NK cells evade mechanisms of cell death after viral 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.