ArticleInfection and immunity2008
Bystander macrophage apoptosis after Mycobacterium tuberculosis H37Ra infection.
Article in Infection and immunity, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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
29 citing papers in PubMed, 53 citations in OpenAlex.
- Article
- The antimycobacterial and healing effect of sorafenib through pro-apoptotic and immunomodulatory activities.Microbiology spectrum · 2026Article
- Jurkat T-Cell Antigen-Independent Elimination of PMA-Activated Neuroblastoma Cells Is Triggered by CCL2/CCR2, Depends Upon Lipid Raft LFA1/ICAM1 Immune Synapses, Is Mediated by m-TRAIL and Is Augmented by the TrkAIII Oncoprotein.International journal of molecular sciences · 2026Article
- CDK1‑induced regulation of p53 phosphorylation at Ser315 mediates cell cycle arrest and apoptosis of macrophages infected with clinical isolates ofMolecular medicine reports · 2026Article
- Bioenergetic reprogramming of macrophages reduces drug tolerance in Mycobacterium tuberculosis.Nature communications · 2025Article
- Host Cell Death and Modulation of Immune Response againstInternational journal of molecular sciences · 2024Review
- Article
- Cytotoxicity of CD19-CAR-NK92 cells is primarily mediated via perforin/granzyme pathway.Cancer immunology, immunotherapy : CII · 2023Article
- Targeting hypoxia-induced tumor stemness by activating pathogen-induced stem cell niche defense.Frontiers in immunology · 2022Article
- The Interplay Between Systemic Inflammation, Oxidative Stress, and Tissue Remodeling in Tuberculosis.Antioxidants & redox signaling · 2021Review
- BiodiversemSphere · 2020Article
- Intelligent Mechanisms of Macrophage Apoptosis Subversion byPathogens (Basel, Switzerland) · 2020Review
- An Army Marches on Its Stomach: Metabolic Intermediates as Antimicrobial Mediators inFrontiers in cellular and infection microbiology · 2020Review
- Article
- Mycobacterial Dormancy Systems and Host Responses in Tuberculosis.Frontiers in immunology · 2017Review
- Low Dose BCG Infection as a Model for Macrophage Activation Maintaining Cell Viability.Journal of immunology research · 2016Article
- Antimycobacterial and HIV-1 Reverse Transcriptase Activity of Julianaceae and Clusiaceae Plant Species from Mexico.Evidence-based complementary and alternative medicine : eCAM · 2015Article
- A caspase-dependent pathway is involved in Wnt/β-catenin signaling promoted apoptosis in Bacillus Calmette-Guerin infected RAW264.7 macrophages.International journal of molecular sciences · 2014Article
- Cell death paradigms in the pathogenesis of Mycobacterium tuberculosis infection.Frontiers in cellular and infection microbiology · 2014Review
- CD271(+) bone marrow mesenchymal stem cells may provide a niche for dormant Mycobacterium tuberculosis.Science translational medicine · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human macrophages infected with Mycobacterium tuberculosis may undergo apoptosis. Macrophage apoptosis contributes to the innate immune response against M. tuberculosis by containing and limiting the growth of mycobacteria and also by depriving the bacillus of its niche cell. Apoptosis of infected macrophages is well documented; however, bystander apoptosis of uninfected macrophages has not been described in the setting of M. tuberculosis. We observed that uninfected human macrophages underwent significant bystander apoptosis 48 and 96 h after they came into contact with macrophages infected with avirulent M. tuberculosis. The bystander apoptosis was significantly greater than the background apoptosis observed in uninfected control cells cultured for the same length of time. There was no evidence of the involvement of tumor necrosis factor alpha, Fas, tumor necrosis factor-related apoptosis-inducing ligand, transforming growth factor beta, Toll-like receptor 2, or MyD88 in contact-mediated bystander apoptosis. This newly described phenomenon may further limit the spread of M. tuberculosis by eliminating the niche cells on which the bacillus relies.
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.