ArticleCell2023
Early cellular mechanisms of type I interferon-driven susceptibility to tuberculosis.
Article in Cell, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 109 papers.
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Who cites it
109 citing papers in PubMed, 123 citations in OpenAlex.
- MNS induces antiviral protection and suppresses inflammation.Annals of medicine · 2026Article
- Mitophagy in pathogenesis and therapeutic implications for infection.Experimental & molecular medicine · 2026Review
- Neutrophil extracellular traps in liver diseases: from molecular mechanisms to therapeutic interventions.Acta pharmacologica Sinica · 2026Review
- Strong, sustained type I IFN signaling acts cell intrinsically to impair IFNγ responses and cause tuberculosis susceptibility.Cell host & microbe · 2026Article
- IFN-α and IFN-β inhibit NLRP1-driven PANoptosis.EMBO reports · 2026Article
- Therapeutic remodeling of the tuberculosis granuloma with 1-methyl-D-tryptophan enhances CD8Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Direct bacterial transcript visualization illuminates spatiotemporal environmental adaptation ofScience advances · 2026Article
- Monocytic niches escape T cell surveillance and promote Mycobacterium tuberculosis persistence in lymph nodes.Immunity · 2026Article
- Network-guided transcriptomics identifies drug-linked host-response biomarkers in tuberculosis disease-state transition.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Airway immune signatures of protection and disease progression in recent human tuberculosis household contacts.Nature immunology · 2026Article
- Restricted MHC-II trafficking inbioRxiv : the preprint server for biology · 2026Article
- Exploratory strain-associated patterns of antiviral transcriptional responses to Zika virus exposure in developing human neural tissue.Genomics & informatics · 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
- 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
- Risk of incident tuberculosis after severe COVID-19: a nationwide cohort study.Nature communications · 2026Article
- NRF2-mediated inhibition of alveolar macrophage MHC II expression during Mycobacterium tuberculosis infection.Cell reports · 2026Article
- Lung mucosal and systemic responses at single-cell resolution in an aerosolized Mycobacterium bovis BCG human challenge model.Cell reports. Medicine · 2026Article
- Diverse infection models demonstrate robust resistance ofbioRxiv : the preprint server for biology · 2026Article
- Characterization of programmed cell death pathways activated in Mycobacterium tuberculosis-infected human macrophages.Cell death discovery · 2026Article
49 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
13 authors at 6 institutions in 1 country.
Funding
Abstract
Mycobacterium tuberculosis (Mtb) causes 1.6 million deaths annually. Active tuberculosis correlates with a neutrophil-driven type I interferon (IFN) signature, but the cellular mechanisms underlying tuberculosis pathogenesis remain poorly understood. We found that interstitial macrophages (IMs) and plasmacytoid dendritic cells (pDCs) are dominant producers of type I IFN during Mtb infection in mice and non-human primates, and pDCs localize near human Mtb granulomas. Depletion of pDCs reduces Mtb burdens, implicating pDCs in tuberculosis pathogenesis. During IFN-driven disease, we observe abundant DNA-containing neutrophil extracellular traps (NETs) described to activate pDCs. Cell-type-specific disruption of the type I IFN receptor suggests that IFNs act on IMs to inhibit Mtb control. Single-cell RNA sequencing (scRNA-seq) indicates that type I IFN-responsive cells are defective in their response to IFNγ, a cytokine critical for Mtb control. We propose that pDC-derived type I IFNs act on IMs to permit bacterial replication, driving further neutrophil recruitment and active tuberculosis disease.
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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.