ReviewNature reviews. Microbiology2010
Evasion of innate immunity by Mycobacterium tuberculosis: is death an exit strategy?
Review in Nature reviews. Microbiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 249 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
249 citing papers in PubMed, 1 synthesis or guideline pooled it, 429 citations in OpenAlex.
- Meta-analysis of active tuberculosis gene expression ascertains host directed drug targets.Frontiers in cellular and infection microbiology · 2022Pooled it
- The Cyclooxygenase 2 Inhibitor Etoricoxib as Adjunctive Therapy in Tuberculosis Impairs Macrophage Control of Mycobacterial Growth.The Journal of infectious diseases · 2024Trial
- Plasma LOX-Products and Monocyte Signaling Is Reduced by Adjunctive Cyclooxygenase-2 Inhibitor in a Phase I Clinical Trial of Tuberculosis Patients.Frontiers in cellular and infection microbiology · 2021Trial
- Article
- Article
- Characterization of programmed cell death pathways activated in Mycobacterium tuberculosis-infected human macrophages.Cell death discovery · 2026Article
- Construction and characterization of novelInfection and immunity · 2026Article
- Immunodominant Tuberculosis Antigens Recognized by Human CD4Cold Spring Harbor perspectives in medicine · 2026Article
- Tissue-specific transcriptional epistasis between Prkn and Lrrk2 during mycobacterial infection.Mammalian genome : official journal of the International Mammalian Genome Society · 2026Article
- The antimycobacterial and healing effect of sorafenib through pro-apoptotic and immunomodulatory activities.Microbiology spectrum · 2026Article
- T cell-macrophage interactions in tuberculosis: What we've got here is failure to communicate.Journal of internal medicine · 2026Review
- Phosphorylation shapes antigen presentation and immune recognition: mechanistic insights and translational perspectives.Frontiers in immunology · 2026Review
- CDK1‑induced regulation of p53 phosphorylation at Ser315 mediates cell cycle arrest and apoptosis of macrophages infected with clinical isolates ofMolecular medicine reports · 2026Article
- Inflammasome Activation Differences Underpin DifferentMedComm · 2025Article
- Article
- Article
- S-nitrosylation-triggered secretion of mycobacterial PknG leads to phosphorylation of SODD to prevent apoptosis of infected macrophages.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Epigenetic regulation of hematopoietic stem cell fate.Trends in cell biology · 2025Review
- Ferroptosis contributes to immunosuppression.Frontiers of medicine · 2025Review
- Exosome-mediated bidirectional immune dysregulation in tuberculosis: proteomic profiling reveals strain-specific strategies of virulent H37Rv and attenuated H37Ra.Frontiers in immunology · 2025Article
189 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
Virulent Mycobacterium tuberculosis inhibits apoptosis and triggers necrosis of host macrophages to evade innate immunity and delay the initiation of adaptive immunity. By contrast, attenuated M. tuberculosis induces macrophage apoptosis, an innate defence mechanism that reduces bacterial viability. In this Opinion article, we describe how virulent M. tuberculosis blocks production of the eicosanoid lipid mediator prostaglandin E(2) (PGE(2)). PGE(2) production by infected macrophages prevents mitochondrial damage and initiates plasma membrane repair, two processes that are crucial for preventing necrosis and inducing apoptosis. Thus, M. tuberculosis-mediated modulation of eicosanoid production determines the death modality of the infected macrophage, which in turn has a substantial impact on the outcome of infection.
Indexed as
Identifiers
What OpenQuestion holds
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.