ArticlePLoS pathogens2017
Natural killer cell-intrinsic type I IFN signaling controls Klebsiella pneumoniae growth during lung infection.
Article in PLoS pathogens, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 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
53 citing papers in PubMed, 87 citations in OpenAlex.
- Wzi modulates immune evasion of hypervirulentVirulence · 2026Article
- An overview of innate cellular immune responses against hypervirulentEmerging microbes & infections · 2026Review
- Source-specific priming of lung NK cells by Pseudomonas LPS enhances resistance to bacterial pneumonia.Signal transduction and targeted therapy · 2026Article
- Type I interferon signaling promotes early innate control ofbioRxiv : the preprint server for biology · 2026Article
- Single-Cell Transcriptome Profiling Reveals the Immune Dysregulation Characteristics of Mice Infected With Brucella abortus.The Journal of infectious diseases · 2026Article
- Gut microbiota metabolite butyric acid alleviatedBurns & trauma · 2026Article
- Advances in infection-immunity mechanisms and molecular regulatory networks in severe pneumonia-associated lung injury.Frontiers in immunology · 2026Review
- Adrenergic receptors: a key determinant of outcomes in bacterial pneumonia and bacterial sepsis-associated acute lung injury/acute respiratory distress syndrome through participation in pulmonary innate immune response.Frontiers in immunology · 2026Review
- NKG2A-mediated immune modulation of natural killer cells by Staphylococcus aureus.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- The dual role of type I interferons in bacterial infections: from immune defense to pathogenesis.mBio · 2025Review
- Impairment of Innate Immunity and Depletion of Vaccine-Induced Memory B and T Cells in the Absence of the Spleen.American journal of hematology · 2025Article
- Type I interferons in bacterial diseases: myeloid cells at the crossroads of protection and pathology.Frontiers in immunology · 2025Review
- Article
- Leukocyte kinetics and bacterial clearance duringAmerican journal of physiology. Lung cellular and molecular physiology · 2025Article
- Isoferulic acid facilitates effective clearance of hypervirulent Klebsiella pneumoniae through targeting capsule.PLoS pathogens · 2025Article
- Natural killer cell effector function is critical for host defense against alcohol-associated bacterial pneumonia.NPJ biofilms and microbiomes · 2024Article
- In vivo single-cell high-dimensional mass cytometry analysis to track the interactions between Klebsiella pneumoniae and myeloid cells.PLoS pathogens · 2024Article
- The Characteristic of Biofilm Formation in ESBL-ProducingThe Canadian journal of infectious diseases & medical microbiology = Journal canadien des maladies infectieuses et de la microbiologie medicale · 2024Article
- Autophagy, cell death, and cytokines inEmerging microbes & infections · 2023Review
- BATF2 enhances proinflammatory cytokine responses in macrophages and improves early host defense against pulmonaryAmerican journal of physiology. Lung cellular and molecular physiology · 2023Article
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 3 countries.
Funding
Abstract
Klebsiella pneumoniae is a significant cause of nosocomial pneumonia and an alarming pathogen owing to the recent isolation of multidrug resistant strains. Understanding of immune responses orchestrating K. pneumoniae clearance by the host is of utmost importance. Here we show that type I interferon (IFN) signaling protects against lung infection with K. pneumoniae by launching bacterial growth-controlling interactions between alveolar macrophages and natural killer (NK) cells. Type I IFNs are important but disparate and incompletely understood regulators of defense against bacterial infections. Type I IFN receptor 1 (Ifnar1)-deficient mice infected with K. pneumoniae failed to activate NK cell-derived IFN-γ production. IFN-γ was required for bactericidal action and the production of the NK cell response-amplifying IL-12 and CXCL10 by alveolar macrophages. Bacterial clearance and NK cell IFN-γ were rescued in Ifnar1-deficient hosts by Ifnar1-proficient NK cells. Consistently, type I IFN signaling in myeloid cells including alveolar macrophages, monocytes and neutrophils was dispensable for host defense and IFN-γ activation. The failure of Ifnar1-deficient hosts to initiate a defense-promoting crosstalk between alveolar macrophages and NK cell was circumvented by administration of exogenous IFN-γ which restored endogenous IFN-γ production and restricted bacterial growth. These data identify NK cell-intrinsic type I IFN signaling as essential driver of K. pneumoniae clearance, and reveal specific targets for future therapeutic exploitations.
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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.