ReviewImmunological reviews2015
TB drug development: immunology at the table.
Review in Immunological reviews, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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
34 citing papers in PubMed.
- Trial
- Antimycobacterial and immunomodulatory activities of sorafenib in a preclinical mouse model of TB infection through CD4Frontiers in immunology · 2025Article
- Drug-TolerantInternational journal of molecular sciences · 2023Article
- Activation of the SigE-SigB signaling pathway by inhibition of the respiratory electron transport chain and its effect on rifampicin resistance in Mycobacterium smegmatis.Journal of microbiology (Seoul, Korea) · 2022Article
- Distinctive roles of translesion polymerases DinB1 and DnaE2 in diversification of the mycobacterial genome through substitution and frameshift mutagenesis.Nature communications · 2022Article
- Central carbon metabolism remodeling as a mechanism to develop drug tolerance and drug resistance inFrontiers in cellular and infection microbiology · 2022Review
- Phosphoenolpyruvate depletion mediates both growth arrest and drug tolerance ofProceedings of the National Academy of Sciences of the United States of America · 2021Article
- Investigating β-Lactam Drug Targets inACS infectious diseases · 2021Article
- Dual inhibition of the terminal oxidases eradicates antibiotic-tolerant Mycobacterium tuberculosis.EMBO molecular medicine · 2021Article
- A Multistress Model for High Throughput Screening Against Nonreplicating Mycobacterium tuberculosis.Methods in molecular biology (Clifton, N.J.) · 2021Article
- Tuberculosis: Past, present and future of the treatment and drug discovery research.Current research in pharmacology and drug discovery · 2021Review
- Molecule Property Analyses of Active Compounds forJournal of medicinal chemistry · 2020Review
- Advances in clinical trial design: Weaving tomorrow's TB treatments.PLoS medicine · 2020Review
- Both Pharmacokinetic Variability and Granuloma Heterogeneity Impact the Ability of the First-Line Antibiotics to Sterilize Tuberculosis Granulomas.Frontiers in pharmacology · 2020Article
- Plakinamine P, A Steroidal Alkaloid with Bactericidal Activity againstMarine drugs · 2019Article
- Transient drug-tolerance and permanent drug-resistance rely on the trehalose-catalytic shift in Mycobacterium tuberculosis.Nature communications · 2019Article
- Differential Culturability ofFrontiers in microbiology · 2019Article
- NADCell reports · 2018Article
- Endothelial lineage-specific interaction of Mycobacterium tuberculosis with the blood and lymphatic systems.Tuberculosis (Edinburgh, Scotland) · 2018Review
- Extreme Drug Tolerance of Mycobacterium tuberculosis in Caseum.Antimicrobial agents and chemotherapy · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Our understanding of the host-pathogen relationship in tuberculosis (TB) can help guide drug discovery in at least two ways. First, the recognition that host immunopathology affects lesional TB drug distribution means that pharmacokinetic evaluation of drug candidates needs to move beyond measurements of drug levels in blood, whole lungs, or alveolar epithelial lining fluid to include measurements in specific types of lesions. Second, by restricting the replication of M. tuberculosis (Mtb) subpopulations in latent TB infection and in active disease, the host immune response puts Mtb into a state associated with phenotypic tolerance to TB drugs selected for their activity against replicating Mtb. This has spurred a major effort to conduct high throughput screens in vitro for compounds that can kill Mtb when it is replicating slowly if at all. Each condition used in vitro to slow Mtb's replication and thereby model the phenotypically drug-tolerant state has advantages and disadvantages. Lead candidates emerging from such in vitro studies face daunting challenges in the design of proof-of-concept studies in animal models. Moreover, some non-replicating subpopulations of Mtb fail to resume replication when plated on agar, although their viability is demonstrable by other means. There is as yet no widely replicated assay in which to screen compounds for their ability to kill this 'viable but non-culturable' subpopulation. Despite these hurdles, drugs that can kill slowly replicating or non-replicating Mtb may offer our best hope for treatment-shortening combination chemotherapy of TB.
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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.