ReviewSeminars in immunology2014
Crosstalk between Mycobacterium tuberculosis and the host cell.
Review in Seminars in immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 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
53 citing papers in PubMed, 85 citations in OpenAlex.
- A copper uptake ABC transport system is essential forEmerging microbes & infections · 2026Article
- Applying prior knowledge of regulatory signaling to investigate macrophage cAMP dynamics during Mycobacterium tuberculosis infection.Scientific reports · 2026Article
- Targeting serine metabolism boosts antimycobacterial immunity during Mycobacterium tuberculosis H37Rv infection.Molecules and cells · 2026Article
- cGAS/STING sensing in dendritic cells discriminates between daptomycin sensitive and resistantiScience · 2026Article
- GPU-accelerated modeling of biological regulatory networks.Scientific reports · 2026Article
- Integrated Approach of Hematological Parameters and Glutathione as Predictors of Pulmonary TB Evolution: A Comprehensive Review.Journal of clinical medicine · 2026Review
- Molecular signaling in coinfection: howFrontiers in immunology · 2026Review
- Downregulated Plasma-Derived Extracellular Vesicle MicroRNAs as Novel Biomarkers for Enhanced Tuberculosis Diagnosis.Journal of immunology research · 2026Article
- Immunomodulatory Nanoparticles Induce Autophagy in Macrophages and ReduceACS infectious diseases · 2025Article
- Structure-based virtual screening andMicrobiology spectrum · 2024Article
- Roles of Lipolytic enzymes inFrontiers in microbiology · 2024Review
- From pathogenesis to antigens: the key to shaping the future of TB vaccines.Frontiers in immunology · 2024Review
- Article
- Structural and functional diversity of bacterial cyclic nucleotide perception by CRP proteins.microLife · 2023Review
- Divergent proinflammatory immune responses associated with the differential susceptibility of cattle breeds to tuberculosis.Frontiers in immunology · 2023Article
- Review
- Proteomics in Biomarker Discovery for Tuberculosis: Current Status and Future Perspectives.Frontiers in microbiology · 2022Review
- Enzyme Characterization of Pro-virulent SntA, a Cell Wall-Anchored Protein ofFrontiers in microbiology · 2022Article
- Itaconate, Arginine, and Gamma-Aminobutyric Acid: A Host Metabolite Triad Protective Against Mycobacterial Infection.Frontiers in immunology · 2022Review
- Macrophage: A Cell With Many Faces and Functions in Tuberculosis.Frontiers in immunology · 2022Review
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
The successful establishment and maintenance of a bacterial infection depend on the pathogen's ability to subvert the host cell's defense response and successfully survive, proliferate, or persist within the infected cell. To circumvent host defense systems, bacterial pathogens produce a variety of virulence factors that potentiate bacterial adherence and invasion and usurp host cell signaling cascades that regulate intracellular microbial survival and trafficking. Mycobacterium tuberculosis, probably one of the most successful pathogens on earth, has coexisted with humanity for centuries, and this intimate and persistent connection between these two organisms suggests that the pathogen has evolved extensive mechanisms to evade the human immune system at multiple levels. While some of these mechanisms are mediated by factors released by M. tuberculosis, others rely on host components that are hijacked to prevent the generation of an effective immune response thus benefiting the survival of M. tuberculosis within the host cell. Here, we describe several of these mechanisms, with an emphasis on the cyclic nucleotide signaling and subversion of host responses that occur at the intracellular level when tubercle bacilli encounter macrophages, a cell that becomes a safe-house for M. tuberculosis although it is specialized to kill most microbes.
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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.