ArticlePLoS pathogens2018
Mononuclear cell dynamics in M. tuberculosis infection provide opportunities for therapeutic intervention.
Article in PLoS pathogens, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 52 citations in OpenAlex.
- Helminth Coinfection Alters Monocyte Activation, Polarization, and Function in LatentJournal of immunology (Baltimore, Md. : 1950) · 2020Trial
- Antigen-experienced airway CD8Science advances · 2026Article
- Monocytic niches escape T cell surveillance and promote Mycobacterium tuberculosis persistence in lymph nodes.Immunity · 2026Article
- The lung tissue environment inbioRxiv : the preprint server for biology · 2026Article
- Impaired IFNγ responsiveness of monocyte-derived lung cells limits immunity to Mycobacterium tuberculosis.Nature communications · 2026Article
- Impaired IFNγ responsiveness of monocyte-derived lung cells limits immunity tobioRxiv : the preprint server for biology · 2025Article
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- In vivo regulation of the monocyte phenotype by Mycobacterium marinum and the ESX-1 type VII secretion system.Scientific reports · 2025Article
- IL-27 attenuated macrophage injury and inflammation induced by Mycobacterium tuberculosis by activating autophagy.In vitro cellular & developmental biology. Animal · 2025Article
- Single-cell analysis revealsScience advances · 2025Article
- Mycobacterium tuberculosis virulence lipid PDIM inhibits autophagy in mice.Nature microbiology · 2024Article
- Metabolically active neutrophils represent a permissive niche for Mycobacterium tuberculosis.Mucosal immunology · 2024Article
- Cytosolic serpins act in a cytoprotective feedback loop that limits ESX-1-dependent death ofmBio · 2024Article
- Mycobacterium tuberculosis Utilizes Serine/Threonine Kinase PknF to Evade NLRP3 Inflammasome-driven Caspase-1 and RIPK3/Caspase-8 Activation in Murine Dendritic Cells.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Heterogeneity in lung macrophage control of Mycobacterium tuberculosis is modulated by T cells.Nature communications · 2024Article
- E3 ubiquitin ligase CBLB regulates innate immune responses and bacterial dissemination during nontuberculous mycobacteria infection.Journal of leukocyte biology · 2024Article
- 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
- Article
- Heterogeneity in lung macrophage control ofbioRxiv : the preprint server for biology · 2023Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Mycobacterium tuberculosis causes chronic infection of mononuclear phagocytes, especially resident (alveolar) macrophages, recruited macrophages, and dendritic cells. Despite the importance of these cells in tuberculosis (TB) pathogenesis and immunity, little is known about the population dynamics of these cells at the sites of infection. We used a combination of congenic monocyte adoptive transfer, and pulse-chase labeling of DNA, to determine the kinetics and characteristics of trafficking, differentiation, and infection of mononuclear phagocytes during the chronic, adaptive immune phase of M. tuberculosis infection in mice. We found that Ly6Chi monocytes traffic rapidly to the lungs, where a subpopulation become Ly6Clo and remain in the lung vascular space, while the remainder migrate into the lung parenchyma and differentiate into Ly6Chi dendritic cells, CD11b+ dendritic cells, and recruited macrophages. As in humans with TB, M. tuberculosis-infected mice have increased numbers of blood monocytes; this is due to increased egress from the bone marrow, and not delayed egress from the blood. Pulse-chase labeling of dividing cells and flow cytometry analysis revealed a T1/2 of ~15 hrs for Ly6Chi monocytes, indicating that they differentiate rapidly upon entry to the parenchyma of infected lungs; in contrast, cells that differentiate from Ly6Chi monocytes turn over more slowly, but diminish in frequency in less than one week. New cells (identified by pulse-chase labeling) acquire bacteria within 1-3 days of appearance in the lungs, indicating that bacteria regularly encounter new cellular niches, even during the chronic stage of infection. Our findings that mononuclear phagocyte populations at the site of M. tuberculosis infection are highly dynamic provide support for specific approaches for host-directed therapies directed at monocytes, including trained immunity, as potential interventions in TB, by replacing cells with limited antimycobacterial capabilities with newly-recruited cells better able to restrict and kill M. tuberculosis.
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