ArticleThe Journal of infectious diseases2021
Harmful Effects of Granulocytic Myeloid-Derived Suppressor Cells on Tuberculosis Caused by Hypervirulent Mycobacteria.
Article in The Journal of infectious diseases, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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.
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Who cites it
14 citing papers in PubMed, 19 citations in OpenAlex.
- Circulating low-density neutrophils as biomarkers of resistance to first-line anti-PD-1/PD-L1 immunotherapy in non-small cell lung cancer.Translational oncology · 2026Article
- Host-directed broad-spectrum immunotherapeutic strategy for respiratory infections: Heat-killed Caulobacter crescentus (HKCC) as an innate-immune based biotherapeutic/postbiotic.PLoS pathogens · 2026Article
- Interleukin-1 receptor antagonist is a conserved early factor for exacerbating tuberculosis susceptibility.bioRxiv : the preprint server for biology · 2025Article
- Considering local immunity for innovative immunomodulatory approaches: pulmonary sepsis as a use case.Frontiers in immunology · 2025Review
- Permissive lung neutrophils facilitate tuberculosis immunopathogenesis in male phagocyte NADPH oxidase-deficient mice.PLoS pathogens · 2024Article
- Immunopathology of PulmonaryInternational journal of molecular sciences · 2024Article
- T cell-specific P2RX7 favors lung parenchymal CD4Cell reports · 2023Article
- Regulated Arginine Metabolism in Immunopathogenesis of a Wide Range of Diseases: Is There a Way to Pass between Scylla and Charybdis?Current issues in molecular biology · 2023Review
- Myeloid-derived suppressor cells are associated with impaired Th1 and Th17 responses and severe pulmonary paracoccidioidomycosis which is reversed by anti-Gr1 therapy.Frontiers in immunology · 2023Article
- Advances in the study of myeloid-derived suppressor cells in infectious lung diseases.Frontiers in immunology · 2023Review
- Direct and indirect effects of pathogenic bacteria on the integrity of intestinal barrier.Therapeutic advances in gastroenterology · 2023Review
- Neutrophils in Tuberculosis: Cell Biology, Cellular Networking and Multitasking in Host Defense.International journal of molecular sciences · 2021Review
- A Murine Model ofFrontiers in microbiology · 2021Article
- P2x7 Receptor Signaling Blockade Reduces Lung Inflammation and Necrosis During Severe Experimental Tuberculosis.Frontiers in cellular and infection microbiology · 2021Article
Corrections and comments
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Authors and funding
15 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe role of myeloid-derived suppressor cells (MDSCs) in patients with severe tuberculosis who suffer from uncontrolled pulmonary inflammation caused by hypervirulent mycobacterial infection remains unclear.
methodsThis issue was addressed using C57BL/6 mice infected with highly virulent Mycobacterium bovis strain MP287/03.
resultsCD11b+GR1int population increased in the bone marrow, blood and lungs during advanced disease. Pulmonary CD11b+GR1int (Ly6GintLy6Cint) cells showed granularity similar to neutrophils and expressed immature myeloid cell markers. These immature neutrophils harbored intracellular bacilli and were preferentially located in the alveoli. T-cell suppression occurred concomitantly with CD11b+GR1int cell accumulation in the lungs. Furthermore, lung and bone marrow GR1+ cells suppressed both T-cell proliferation and interferon γ production in vitro. Anti-GR1 therapy given when MDSCs infiltrated the lungs prevented expansion and fusion of primary pulmonary lesions and the development of intragranulomatous caseous necrosis, along with increased mouse survival and partial recovery of T-cell function. Lung bacterial load was reduced by anti-GR1 treatment, but mycobacteria released from the depleted cells proliferated extracellularly in the alveoli, forming cords and clumps.
conclusionsGranulocytic MDSCs massively infiltrate the lungs during infection with hypervirulent mycobacteria, promoting bacterial growth and the development of inflammatory and necrotic lesions, and are promising targets for host-directed therapies.
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