ArticleMucosal immunology2021
Granulocytes act as a niche for Mycobacterium tuberculosis growth.
Article in Mucosal immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
What it found
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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.
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Who cites it
60 citing papers in PubMed, 94 citations in OpenAlex.
- Strong, sustained type I IFN signaling acts cell intrinsically to impair IFNγ responses and cause tuberculosis susceptibility.Cell host & microbe · 2026Article
- Airway immune signatures of protection and disease progression in recent human tuberculosis household contacts.Nature immunology · 2026Article
- Neutrophils and tuberculosis - insights into immunobiology and pathogenesis.Molecular biology reports · 2026Review
- Review
- The host immune response to Mycobacterium tuberculosis determining protection or disease progression.Nature immunology · 2026Review
- Interstitial and recruited macrophages prevent tuberculosis relapse by limiting immune evasion.EMBO molecular medicine · 2026Article
- Ly6GeLife · 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
- T cell-macrophage interactions in tuberculosis: What we've got here is failure to communicate.Journal of internal medicine · 2026Review
- Mycobacterium tuberculosis biology, pathogenicity and interaction with the host.Nature reviews. Microbiology · 2025Review
- Type I IFN drives neutrophil swarming, impeding lung T cell-macrophage interactions and TB control.The Journal of experimental medicine · 2025Article
- Essential redundancies fuel Mycobacterium tuberculosis adaptation to the host.PLoS pathogens · 2025Review
- Mycobacterium tuberculosis-specific T cells restrain anti-cancer drug-induced neutrophilic lung inflammation in tuberculosis.Nature communications · 2025Article
- Early and opposing neutrophil and CD4 T cell responses shape pulmonary tuberculosis pathology.The Journal of experimental medicine · 2025Article
- APOE protects against severe infection with Mycobacterium tuberculosis by restraining production of neutrophil extracellular traps.PLoS pathogens · 2025Article
- Protein Kinase C δ: a critical hub regulating macrophage immunomodulatory functions duringbioRxiv : the preprint server for biology · 2025Article
- Interleukin-1 receptor antagonist is a conserved early factor for exacerbating tuberculosis susceptibility.bioRxiv : the preprint server for biology · 2025Article
- Pathogenic role for CD101-negative neutrophils in the type I interferon-mediated immunopathogenesis of tuberculosis.Cell reports · 2025Article
- The role of neutrophil response in lung damage and post-tuberculosis lung disease: a translational narrative review.Frontiers in immunology · 2025Review
- Mycobacterium tuberculosis virulence lipid PDIM inhibits autophagy in mice.Nature microbiology · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Granulocyte recruitment to the pulmonary compartment is a hallmark of progressive tuberculosis (TB). This process is well-documented to promote immunopathology, but can also enhance the replication of the pathogen. Both the specific granulocytes responsible for increasing mycobacterial burden and the underlying mechanisms remain obscure. We report that the known immunomodulatory effects of these cells, such as suppression of protective T-cell responses, play a limited role in altering host control of mycobacterial replication in susceptible mice. Instead, we find that the adaptive immune response preferentially restricts the burden of bacteria within monocytes and macrophages compared to granulocytes. Specifically, mycobacteria within inflammatory lesions are preferentially found within long-lived granulocytes that express intermediate levels of the Ly6G marker and low levels of antimicrobial genes. These cells progressively accumulate in the lung and correlate with bacterial load and disease severity, and the ablation of Ly6G-expressing cells lowers mycobacterial burden. These observations suggest a model in which dysregulated granulocytic influx promotes disease by creating a permissive intracellular niche for mycobacterial growth and persistence.
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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.