ArticleNature microbiology2025
ATG5 suppresses type I IFN-dependent neutrophil effector functions during Mycobacterium tuberculosis infection in mice.
Article in Nature microbiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed.
- Sorting nexin 5 deficiency impairs MHC class II antigen presentation and inflammatory responses during tuberculosis.Journal of immunology (Baltimore, Md. : 1950) · 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
- 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
- Deubiquitinase USP15 restricts LC3-dependent targeting ofAutophagy · 2026Article
- Deficiency of interleukin-40 prevents intestinal damage in experimental necrotizing enterocolitis by inhibiting NETosis.Cell communication and signaling : CCS · 2026Article
- Sorting nexin 5 mediates antigen presentation and immunity againstbioRxiv : the preprint server for biology · 2026Article
- Exploring Host-driven Immunopathological Factors Developing Severe Tuberculosis: Insights from Comparative Mouse Models.International journal of biological sciences · 2026Article
- Cell death pathways in response toInfection and immunity · 2025Review
- Neutrophil extracellular traps: emerging drivers and therapeutic targets in abdominal aortic aneurysm pathogenesis.Experimental biology and medicine (Maywood, N.J.) · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
Abstract
Inflammation is critical for controlling infections but can cause disease when unchecked. During Mycobacterium tuberculosis (Mtb) infection, neutrophil-dominated inflammation is associated with exacerbated disease. ATG5 expression by neutrophils mediates autophagy-independent control of infection but mechanistic understanding of how this regulates protective neutrophil function is lacking. Using genetic mouse models along with in vivo and in vitro infection systems, we report herein that ATG5 is required in neutrophils to suppress type I interferon-induced PAD4-mediated histone citrullination and neutrophil extracellular trap (NET) release. In addition, ATG5 suppresses type I interferon-induced CXCL2 secretion and neutrophil swarming during Mtb infection. Elevated type I IFN signalling and NET release contribute to the early susceptibility of Atg5
Indexed as
Identifiers
40374743What 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.