ArticleNature communications2020
Type I IFN exacerbates disease in tuberculosis-susceptible mice by inducing neutrophil-mediated lung inflammation and NETosis.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02715271 (Study of TB Lesions Obtained in Surgery), which is not on this map. Cited by 152 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Study of TB Lesions Obtained in Surgery: in Search of Best Biomarkers Correlating With TB Pathology, Clinical Features, MDR Cases and Prognostic
Who cites it
152 citing papers in PubMed, 1 synthesis or guideline pooled it, 216 citations in OpenAlex.
- Systematic review of innate immune responses againstFrontiers in immunology · 2024Pooled it
- Therapy of allergic rhinitis using ribavirin spray to clear nasal commensal viruses.Signal transduction and targeted therapy · 2026Trial
- Host-pathogen interactions in tuberculosis: from immunological mechanisms to translational applications.Cell insight · 2026Review
- Strong, sustained type I IFN signaling acts cell intrinsically to impair IFNγ responses and cause tuberculosis susceptibility.Cell host & microbe · 2026Article
- Monocytic niches escape T cell surveillance and promote Mycobacterium tuberculosis persistence in lymph nodes.Immunity · 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
- IFN𝛾 and IFN𝛾 mimetics prevent IFN-I-mediated TB susceptibility by regulating iron metabolism and lipid peroxidation.bioRxiv : the preprint server for biology · 2026Article
- The study of immunological markers in tuberculosis across animal models and its translation to human research.Lab animal · 2026Review
- NETosis associates with human TB lung tissue destruction and disease pathogenesis.EMBO molecular medicine · 2026Article
- Integrative single-cell profiling and explainable AI identify monocyte-metabolic signatures as diagnostic biomarkers and candidate therapeutic targets in tuberculosis.Archives of microbiology · 2026Article
- Type I interferon signaling in hematopoietic cells impairs neutrophil antibacterial function in the middle ear during viral co-infection.Cell reports. Medicine · 2026Article
- Immune endotypes in tuberculosis: Keys to decoding disease complexity.Journal of internal medicine · 2026Review
- The host immune response to Mycobacterium tuberculosis determining protection or disease progression.Nature immunology · 2026Review
- Neutrophils repurpose the nucleolus as a cytokine reservoir and secretory organelle.bioRxiv : the preprint server for biology · 2026Article
- Elimination of senescent cells with senolytic drugs as adjunctive host-directed therapy reduces tuberculosis progression in mice.Nature communications · 2026Article
- Clinical and transcriptomic risk factors for post-tuberculosis lung disease in a cohort of Kenyan adults.American journal of respiratory and critical care medicine · 2026Observational
- Context-specific roles for IL-17 in tuberculosis.PLoS pathogens · 2026Review
- Single-cell profiling reveals that dynamic lung immune responses distinguish protection from susceptibility to tuberculosis.PLoS pathogens · 2026Article
- Post-TB lung disease: pathogenesis, host-directed therapies, and the C3HeB/FeJ model for pre-clinical advances.Infection and immunity · 2026Review
92 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
19 authors at 6 institutions in 4 countries.
Funding
Abstract
Tuberculosis (TB) is a leading cause of mortality due to infectious disease, but the factors determining disease progression are unclear. Transcriptional signatures associated with type I IFN signalling and neutrophilic inflammation were shown to correlate with disease severity in mouse models of TB. Here we show that similar transcriptional signatures correlate with increased bacterial loads and exacerbate pathology during Mycobacterium tuberculosis infection upon GM-CSF blockade. Loss of GM-CSF signalling or genetic susceptibility to TB (C3HeB/FeJ mice) result in type I IFN-induced neutrophil extracellular trap (NET) formation that promotes bacterial growth and promotes disease severity. Consistently, NETs are present in necrotic lung lesions of TB patients responding poorly to antibiotic therapy, supporting the role of NETs in a late stage of TB pathogenesis. Our findings reveal an important cytokine-based innate immune effector network with a central role in determining the outcome of M. tuberculosis infection.
Indexed as
Identifiers
What OpenQuestion holds
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.