ArticlePloS one2011
Interferon gamma activated macrophages kill mycobacteria by nitric oxide induced apoptosis.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 138 papers, 1 of them a synthesis that pooled it.
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Who cites it
138 citing papers in PubMed, 1 synthesis or guideline pooled it, 278 citations in OpenAlex.
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- Species-specific iNOS expression distinguishes epithelial and myeloid IFNγ responses in tuberculosis.bioRxiv : the preprint server for biology · 2026Article
- Prior Exposure of Airway Epithelial Cells to Mycobacteria Reduces Subsequent <italic>Mycobacterium tuberculosis</italic> Infection and Resulting Inflammation.Journal of innate immunity · 2026Article
- IFN-γ and IL-6 as Key Predicting Biomarkers for Active TB Among PLWH: Results from Four Machine Learning Methods.International journal of general medicine · 2026Article
- Impact of L-arginine and L-citrulline supplementation on macrophage responses toFrontiers in immunology · 2026Article
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- Modeling immune responses of cattle tomSphere · 2025Article
- Alveolar macrophage transcriptional signatures associated with resistance to TST/IGRA conversion following Mycobacterium tuberculosis exposure.BMC genomics · 2025Article
- c-Myc Inhibits Macrophage Antimycobacterial Response in Mycobacterium tuberculosis Infection.The Journal of infectious diseases · 2025Article
- An unusual genetic switch controlsbioRxiv : the preprint server for biology · 2025Article
- IL-27 signaling limits the diversity of antigen-specific T cells and interferes with protection induced by BCG vaccination.Tuberculosis (Edinburgh, Scotland) · 2025Article
- Inflammation and dyslipidaemia in combined diabetes and tuberculosis; a cohort study.iScience · 2025Article
- c-Myc inhibits macrophage antimycobacterial response inbioRxiv : the preprint server for biology · 2025Article
- I just hurt myself out in the garden… right?Breathe (Sheffield, England) · 2025Article
- Tax1bp1 enhances bacterial virulence and promotes inflammatory responses duringbioRxiv : the preprint server for biology · 2024Article
78 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
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Mycobacterium tuberculosis is an intracellular pathogen of macrophages and escapes the macrophages' bactericidal effectors by interfering with phagosome-lysosome fusion. IFN-γ activation renders the macrophages capable of killing intracellular mycobacteria by overcoming the phagosome maturation block, nutrient deprivation and exposure to microbicidal effectors including nitric oxide (NO). While the importance about NO for the control of mycobacterial infection in murine macrophages is well documented, the underlying mechanism has not been revealed yet. In this study we show that IFN-γ induced apoptosis in mycobacteria-infected macrophages, which was strictly dependent on NO. Subsequently, NO-mediated apoptosis resulted in the killing of intracellular mycobacteria independent of autophagy. In fact, killing of mycobacteria was susceptible to the autophagy inhibitor 3-methyladenine (3-MA). However, 3-MA also suppressed NO production, which is an important off-target effect to be considered in autophagy studies using 3-MA. Inhibition of caspase 3/7 activation, as well as NO production, abolished apoptosis and elimination of mycobacteria by IFN-γ activated macrophages. In line with the finding that drug-induced apoptosis kills intracellular mycobacteria in the absence of NO, we identified NO-mediated apoptosis as a new defense mechanism of activated macrophages against M. tuberculosis.
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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.