ReviewImmunological reviews2011
Mycobacterium tuberculosis and the intimate discourse of a chronic infection.
Review in Immunological reviews, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 156 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
156 citing papers in PubMed, 279 citations in OpenAlex.
- Transcriptional control of asparagine utilization regulates mycobacterial pH-driven adaptation at the host-pathogen crossroads.The Journal of biological chemistry · 2026Article
- γδ T Cells at the Crossroads of Tuberculosis and COPD: From Early Immunity to Tissue Remodeling.International journal of molecular sciences · 2026Review
- Nanotechnology-Enabled Strategies to Overcome Antibiotic Resistance in Respiratory Infections: Mechanisms, Platforms, and Translational Challenges.Biomedicines · 2026Review
- Integrative single-cell profiling and explainable AI identify monocyte-metabolic signatures as diagnostic biomarkers and candidate therapeutic targets in tuberculosis.Archives of microbiology · 2026Article
- Non-canonical peptidoglycan cross-linking is essential forbioRxiv : the preprint server for biology · 2026Article
- The lipid language of tuberculosis:mBio · 2026Review
- A co-evolutionary perspective on humans andeLife · 2026Review
- The regulatory role of the Notch signaling pathway in mitophagy and macrophage-mediated elimination of Mycobacterium bovis bacillus Calmette-Guérin.BMC infectious diseases · 2025Article
- Article
- A bacterial effector manipulates host lysosomal protease activity-dependent plasticity in cell death modalities to facilitate infection.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Deciphering tuberculosis: lysosome-centric insights into pathogenesis and therapies.Frontiers in cellular and infection microbiology · 2025Review
- Molecular and microbiological methods for the identification of nonreplicating Mycobacterium tuberculosis.PLoS pathogens · 2024Review
- Review
- Article
- The Role of mRNA Alternative Splicing in Macrophages Infected withMolecules (Basel, Switzerland) · 2024Review
- CytochromeRSC medicinal chemistry · 2024Review
- TNF in Human Tuberculosis: A Double-Edged Sword.Immune network · 2024Review
- Understanding the development of tuberculous granulomas: insights into host protection and pathogenesis, a review in humans and animals.Frontiers in immunology · 2024Review
- Recent Biochemical Advances in Antitubercular Drugs: Challenges and Future.Current topics in medicinal chemistry · 2024Review
- Mycobacterium tuberculosis β-lactamase variant reduces sensitivity to ampicillin/avibactam in a zebrafish-Mycobacterium marinum model of tuberculosis.Scientific reports · 2023Article
96 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
1 author at 1 institution in 1 country.
Funding
Abstract
Mycobacterium tuberculosis is an extremely successful pathogen that demonstrates the capacity to modulate its host both at the cellular and tissue levels. At the cellular level, the bacterium enters its host macrophage and arrests phagosome maturation, thus avoiding many of the microbicidal responses associated with this phagocyte. Nonetheless, the intracellular environment places certain demands on the pathogen, which, in response, senses the environmental shifts and upregulates specific metabolic programs to allow access to nutrients, minimize the consequences of stress, and sustain infection. Despite its intracellular niche, Mycobacterium tuberculosis demonstrates a marked capacity to modulate the tissues surrounding infected cells through the release of potent, bioactive cell wall constituents. These cell wall lipids are released from the host cell by an exocytic process and induce physiological changes in neighboring phagocytes, which drives formation of a granuloma. This tissue response leads to the generation and accumulation of caseous debris and the progression of the human tuberculosis granuloma. Completion of the life cycle of tuberculosis requires damaging the host to release infectious bacteria into the airways to spread the infection. This damage reflects the pathogen's ability to subvert the host's innate and acquired immune responses to its own nefarious ends.
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.