ReviewJournal of leukocyte biology2018
Mycobacterium tuberculosis: Rewiring host cell signaling to promote infection.
Review in Journal of leukocyte biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
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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
35 citing papers in PubMed, 76 citations in OpenAlex.
- Organelle interplay in host responses and mycobacterial resilience.EMBO reports · 2026Review
- Mechanisms ofBreathe (Sheffield, England) · 2026Review
- Fighting the invader: strategies against intracellular bacteria.Frontiers in pharmacology · 2026Review
- Mycobacterium tuberculosis curli pili (MTP) facilitates pathogenicity by modulating oxidative phosphorylation and carbon flux during early infection of A549 epithelial cells.Metabolomics : Official journal of the Metabolomic Society · 2025Article
- Mycobacterium tuberculosis triggers reduced inflammatory cytokine responses and virulence in mice lacking Tax1bp1.PLoS pathogens · 2025Article
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- Advances in Host-Pathogen Interactions in Tuberculosis: Emerging Strategies for Therapeutic Intervention.International journal of molecular sciences · 2025Review
- Deletion of ESX-3 and ESX-4 secretion systems in Mycobacterium abscessus results in highly impaired pathogenicity.Communications biology · 2025Article
- Tax1bp1 enhances bacterial virulence and promotes inflammatory responses duringbioRxiv : the preprint server for biology · 2024Article
- Mycobacterium tuberculosis: The Mechanism of Pathogenicity, Immune Responses, and Diagnostic Challenges.Journal of clinical laboratory analysis · 2024Review
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- ZebrafishLife science alliance · 2024Article
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- Article
- Different modalities of host cell death and their impact onAmerican journal of physiology. Cell physiology · 2022Review
- microRNAs associated with the pathogenesis and their role in regulating various signaling pathways duringFrontiers in cellular and infection microbiology · 2022Review
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- Integrative genomics of the mammalian alveolar macrophage response to intracellular mycobacteria.BMC genomics · 2021Article
- Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The ability of Mycobacterium tuberculosis to cause disease hinges upon successfully thwarting the innate defenses of the macrophage host cell. The pathogen's trump card is its armory of virulence factors that throw normal host cell signaling into disarray. This process of subverting the macrophage begins upon entry into the cell, when M. tuberculosis actively inhibits the fusion of the bacilli-laden phagosomes with lysosomes. The pathogen then modulates an array of host signal transduction pathways, which dampens the macrophage's host-protective cytokine response, while simultaneously adapting host cell metabolism to stimulate lipid body accumulation. Mycobacterium tuberculosis also renovates the surface of its innate host cells by altering the expression of key molecules required for full activation of the adaptive immune response. Finally, the pathogen coordinates its exit from the host cell by shifting the balance from the host-protective apoptotic cell death program toward a lytic form of host cell death. Thus, M. tuberculosis exploits its extensive repertoire of virulence factors in order to orchestrate the infection process to facilitate its growth, dissemination, and entry into latency. This review offers critical insights into the most recent advances in our knowledge of how M. tuberculosis manipulates host cell signaling. An appreciation of such interactions between the pathogen and host is critical for guiding novel therapies and understanding the factors that lead to the development of active disease in only a subset of exposed individuals.
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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.