ArticleImmunity2008
Tumor necrosis factor signaling mediates resistance to mycobacteria by inhibiting bacterial growth and macrophage death.
Article in Immunity, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 189 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
189 citing papers in PubMed, 379 citations in OpenAlex.
- Tim-3-expressing CD4+ and CD8+ T cells in human tuberculosis (TB) exhibit polarized effector memory phenotypes and stronger anti-TB effector functions.PLoS pathogens · 2012Trial
- Host-pathogen interactions in tuberculosis: from immunological mechanisms to translational applications.Cell insight · 2026Review
- Transmembrane delivery of antimicrobial peptides by engineered eCIS into macrophages for intracellular mycobacteria elimination.Science advances · 2026Article
- Protective versus deleterious roles of pyroptosis in Mycobacterium avium and Mycobacterium marinum infections.Cell death & disease · 2026Article
- Autoimmune Diseases and Mycobacterial Infection.Diseases (Basel, Switzerland) · 2026Review
- Telomere shortening correlates with immune dysregulation and severity in pulmonary tuberculosis.BMC pulmonary medicine · 2026Article
- Macrophage adaptation to hypoxia in the tuberculous granuloma potentiates mycobacterium-induced mitochondrial damage and granuloma necrosis.bioRxiv : the preprint server for biology · 2026Article
- Factors Associated with Active Tuberculosis Disease in Patients with Lung Cancer Following Immune Checkpoint Blockade Therapy: A Retrospective Cohort Study and Case Reports.Infection and drug resistance · 2026Article
- A quadral biosignature of IFN-γ, IL-2, IL-12 and IP-10 increases the diagnostic potential for latent tuberculosis among diabetic patients in Uganda.BMC immunology · 2025Article
- The impact of air pollution on active tuberculosis development from latent tuberculosis infection in rural China: 10-year follow-up of a cohort study.ERJ open research · 2025Article
- Beyond additive effects: examining the combined impact of air pollutant interactions on pulmonary tuberculosis in China.BMC public health · 2025Article
- Review
- Metabolic dysfunction impairs Mycobacterium tuberculosis-specific cytokine and chemokine responses in latent tuberculosis and type 2 diabetes mellitus.Scientific reports · 2025Article
- A granulin-positive macrophage subtype in mycobacterial granulomas alleviates tissue damage by limiting excessive inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- A CARD9 deficiency mouse model recapitulates human chronic CNS candidiasis identifying defective monocytic cell responses in immunopathogenesis.JCI insight · 2025Article
- Review
- Role of Tumor Necrosis Factor in Tuberculosis.Biomolecules · 2025Review
- 3D Hydrogel Culture System Recapitulates Key Tuberculosis Phenotypes and Demonstrates Pyrazinamide Efficacy.Advanced healthcare materials · 2025Article
- Ameliorative role of camel protein hydrolysates diet against alkaline stress in Oreochrmis niloticus: Hematology, immune responses and their regulating genes expression, and histopathological assays.Veterinary research communications · 2025Article
- Host Immune Response toJournal of inflammation research · 2025Review
129 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Tumor necrosis factor (TNF), a key effector in controlling tuberculosis, is thought to exert protection by directing formation of granulomas, organized aggregates of macrophages and other immune cells. Loss of TNF signaling causes progression of tuberculosis in humans, and the increased mortality of Mycobacterium tuberculosis-infected mice is associated with disorganized necrotic granulomas, although the precise roles of TNF signaling preceding this endpoint remain undefined. We monitored transparent Mycobacterium marinum-infected zebrafish live to conduct a stepwise dissection of how TNF signaling operates in mycobacterial pathogenesis. We found that loss of TNF signaling caused increased mortality even when only innate immunity was operant. In the absence of TNF, intracellular bacterial growth and granuloma formation were accelerated and was followed by necrotic death of overladen macrophages and granuloma breakdown. Thus, TNF is not required for tuberculous granuloma formation, but maintains granuloma integrity indirectly by restricting mycobacterial growth within macrophages and preventing their necrosis.
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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.