ArticleCell host & microbe2024
Type I IFN-mediated NET release promotes Mycobacterium tuberculosis replication and is associated with granuloma caseation.
Article in Cell host & microbe, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed.
- Mitophagy in pathogenesis and therapeutic implications for infection.Experimental & molecular medicine · 2026Review
- Host-pathogen interactions in tuberculosis: from immunological mechanisms to translational applications.Cell insight · 2026Review
- Assembled Hyaluronic Acid Therapeutics for Targeting M1 Macrophages and Regulating Immune Homeostasis for Ulcerative Colitis Treatment.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- IFNAR1-dependent metabolic circuit drives pathogenic neutrophil activation in chronic mucosal inflammation.Signal transduction and targeted therapy · 2026Article
- Discovery and validation of novel plasma protein biomarkers for severe tuberculosis patients.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Strong, sustained type I IFN signaling acts cell intrinsically to impair IFNγ responses and cause tuberculosis susceptibility.Cell host & microbe · 2026Article
- Direct bacterial transcript visualization illuminates spatiotemporal environmental adaptation ofScience advances · 2026Article
- TLR7/9 and type I interferon signaling reprogram neutrophil NET responses and impair antibacterial defense in systemic lupus erythematosus.Cell press blue · 2026Article
- IFN𝛾 and IFN𝛾 mimetics prevent IFN-I-mediated TB susceptibility by regulating iron metabolism and lipid peroxidation.bioRxiv : the preprint server for biology · 2026Article
- NETosis associates with human TB lung tissue destruction and disease pathogenesis.EMBO molecular medicine · 2026Article
- Mitochondrial STAT3-mediated suppression of apoptosis constrains antimycobacterial immunity.bioRxiv : the preprint server for biology · 2026Article
- Cell death crosstalk in NET-Driven inflammation: mechanisms, disease contexts, and therapeutic perspectives.Biomarker research · 2026Review
- NRF2-mediated inhibition of alveolar macrophage MHC II expression during Mycobacterium tuberculosis infection.Cell reports · 2026Article
- CSF2 drives radiation-induced lung injury by eliciting PADI4-high pathogenic neutrophils.Journal of translational medicine · 2026Article
- Characterization of programmed cell death pathways activated in Mycobacterium tuberculosis-infected human macrophages.Cell death discovery · 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
- IFNγ blockade in Mycobacterium tuberculosis infected macaques alters the granuloma environment but not bacterial control.Nature communications · 2026Article
- Strain-dependent disease progression and necrotizing granuloma formation in a murine model induced by virulent strains ofMicrobiology spectrum · 2026Article
Corrections and comments
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Authors and funding
17 authors.
Funding
Abstract
Neutrophils are the most abundant cell type in the airways of tuberculosis patients. Mycobacterium tuberculosis (Mtb) infection induces the release of neutrophil extracellular traps (NETs); however, the molecular regulation and impact of NET release on Mtb pathogenesis are unknown. We find that during Mtb infection in neutrophils, PAD4 citrullinates histones to decondense chromatin that gets released as NETs in a manner that can maintain neutrophil viability and promote Mtb replication. Type I interferon promotes the formation of chromatin-containing vesicles that allow NET release without compromising plasma membrane integrity. Analysis of nonhuman primate granulomas supports a model where neutrophils are exposed to type I interferon from macrophages as they migrate into the granuloma, thereby enabling the release of NETs associated with necrosis and caseation. Our data reveal NET release as a promising target to inhibit Mtb pathogenesis.
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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.