ArticleThe Journal of experimental medicine2025
Type I IFN drives neutrophil swarming, impeding lung T cell-macrophage interactions and TB control.
Article in The Journal of experimental medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- 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
- In tuberculosis, the neutrophil is neutral in name alone.Nature immunology · 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
- 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 host immune response to Mycobacterium tuberculosis determining protection or disease progression.Nature immunology · 2026Review
- Modulation of Ferroptosis During EarlybioRxiv : the preprint server for biology · 2026Article
- Neutrophils repurpose the nucleolus as a cytokine reservoir and secretory organelle.bioRxiv : the preprint server for biology · 2026Article
- TGFβ primes alveolar-like macrophages to induce type I IFN following TLR2 activation.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- HowVaccines · 2026Review
- Context-specific roles for IL-17 in tuberculosis.PLoS pathogens · 2026Review
- Host-response biomarkers for precision tuberculosis: from immune transcriptomic signatures to clinical risk stratification.Frontiers in cell and developmental biology · 2026Review
- Activation of nuclear receptors correlates with tuberculosis severity and is a target for host-directed therapy.Frontiers in cellular and infection microbiology · 2025Article
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
The early immune mechanisms determining Mycobacterium tuberculosis infection outcome are unclear. Using bulk and scRNA-seq over the first weeks of infection, we describe an unexpected, higher early pulmonary type I IFN response in relatively resistant C57BL/6 as compared with highly TB-susceptible C3HeB/FeJ mice. C57BL/6 mice showed pronounced early monocyte-derived macrophage (MDM) accumulation and extensive CD4+ T cell-MDM interactions in lung lesions, accompanied by high expression of T cell-attractant chemokines by MDMs. Conversely, lesions in C3HeB/FeJ mice were dominated by neutrophils with high expression of pro-inflammatory chemokines, from which CD4+ T cells were spatially segregated. Early type I IFN signaling blockade reduced bacterial load and neutrophil swarming within early TB lesions while increasing CD4+ T cell numbers in both C57BL/6 and C3HeB/FeJ mice, with later more pronounced effects on bacterial load in C3HeB/FeJ mice. These data suggest that early type I IFN signaling during M. tuberculosis infection favors neutrophil accumulation and limits CD4+ T cell infiltration into developing lesions.
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