ArticleCell host & microbe2012
Mycobacterium tuberculosis inhibits neutrophil apoptosis, leading to delayed activation of naive CD4 T cells.
Article in Cell host & microbe, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers.
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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.
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Who cites it
106 citing papers in PubMed, 190 citations in OpenAlex.
- Neutrophils and tuberculosis - insights into immunobiology and pathogenesis.Molecular biology reports · 2026Review
- Mitochondrial STAT3-mediated suppression of apoptosis constrains antimycobacterial immunity.bioRxiv : the preprint server for biology · 2026Article
- Lung mucosal and systemic responses at single-cell resolution in an aerosolized Mycobacterium bovis BCG human challenge model.Cell reports. Medicine · 2026Article
- HowVaccines · 2026Review
- Inhalational therapy of pulmonary infectionActa pharmaceutica Sinica. B · 2026Article
- Protein-Mediated Virulence in Mycobacterium tuberculosis.Advances in experimental medicine and biology · 2026Review
- T cell-macrophage interactions in tuberculosis: What we've got here is failure to communicate.Journal of internal medicine · 2026Review
- Inflammasome Activation Differences Underpin DifferentMedComm · 2025Article
- Real-time visualization reveals Mycobacterium tuberculosis ESAT-6 disrupts phagosome-like compartment via fibril-mediated vesiculation.Cell reports · 2025Article
- Dendritic Cell Vaccine Harboring Inactivated Mycobacteria Induces Immune Protection Against Tuberculosis in Murine Models and is Well Tolerated in Humans.Small science · 2025Article
- Unveiling the immunological landscape of disseminated tuberculosis: a single-cell transcriptome perspective.Frontiers in immunology · 2025Article
- Mycobacterium tuberculosis resides in lysosome-poor monocyte-derived lung cells during chronic infection.PLoS pathogens · 2024Article
- CpsA mediates infection of recruited lung myeloid cells by Mycobacterium tuberculosis.Cell reports · 2024Article
- From pathogenesis to antigens: the key to shaping the future of TB vaccines.Frontiers in immunology · 2024Review
- Pathogenicity and virulence ofVirulence · 2023Review
- Combination of MCL-1 and BCL-2 inhibitors is a promising approach for a host-directed therapy for tuberculosis.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2023Article
- Advances of Long Non-Coding RNAs as Potential Biomarkers for Tuberculosis: New Hope for Diagnosis?Pharmaceutics · 2023Review
- Clinical manifestations and immune response to tuberculosis.World journal of microbiology & biotechnology · 2023Review
- Microbes and the fate of neutrophils.Immunological reviews · 2023Review
- Study of the Rv1417 and Rv2617c Membrane Proteins and Their Interactions with Nicotine Derivatives as Potential Inhibitors of Erp Virulence-Associated Factor inBiomolecules · 2023Article
46 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
4 authors at 2 institutions in 1 country.
Funding
Abstract
Mycobacterium tuberculosis promotes its replication by inhibiting the apoptosis of infected macrophages. A proapoptotic M. tuberculosis mutant lacking nuoG, a subunit of the type I NADH dehydrogenase complex, exhibits attenuated growth in vivo, indicating that this virulence mechanism is essential. We show that M. tuberculosis also suppresses neutrophil apoptosis. Compared to wild-type, the nuoG mutant spread to a larger number of lung phagocytic cells. Consistent with the shorter lifespan of infected neutrophils, infection with the nuoG mutant resulted in fewer bacteria per infected neutrophil, accelerated bacterial acquisition by dendritic cells, earlier trafficking of these dendritic cells to lymph nodes, and faster CD4 T cell priming. Neutrophil depletion abrogated accelerated CD4 T cell priming by the nuoG mutant, suggesting that inhibiting neutrophil apoptosis delays adaptive immunity in tuberculosis. Thus, pathogen modulation of apoptosis is beneficial at multiple levels, and enhancing phagocyte apoptosis promotes CD4 as well as CD8 T cell responses.
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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.