ArticleNature microbiology2023
Autophagy restricts Mycobacterium tuberculosis during acute infection in mice.
Article in Nature microbiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 58 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.
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Who cites it
58 citing papers in PubMed, 93 citations in OpenAlex.
- Canonical and noncanonical autophagy in immunity.Immunity · 2026Review
- Restricted MHC-II trafficking inbioRxiv : the preprint server for biology · 2026Article
- Diverse infection models demonstrate robust resistance ofbioRxiv : the preprint server for biology · 2026Article
- CMPK2 restrictsbioRxiv : the preprint server for biology · 2026Article
- Circulating metabolites associated with protection against Mycobacterium tuberculosis infection and inhibition of mycobacterial growth.Communications biology · 2026Article
- HowVaccines · 2026Review
- Borrelia burgdorferi sensu lato Employs Several Escape Mechanisms to Bypass the Human Defense System.European journal of immunology · 2026Review
- Deubiquitinase USP15 restricts LC3-dependent targeting ofAutophagy · 2026Article
- The lipid language of tuberculosis:mBio · 2026Review
- Article
- Membrane atg8ylation and autophagy in protection against Mycobacterium tuberculosis.Journal of immunology (Baltimore, Md. : 1950) · 2026Review
- Mycobacterial α-glucans hijack dectin-1 to facilitate intracellular bacterial survival.Science immunology · 2026Article
- Membrane microdomains are crucial forScience advances · 2026Article
- Mycobacterium tuberculosis biology, pathogenicity and interaction with the host.Nature reviews. Microbiology · 2025Review
- The role of TRIM proteins in the pathogenesis of mycobacterium tuberculosis.Biology direct · 2025Review
- Cell death pathways in response toInfection and immunity · 2025Review
- Host-directed therapeutic targets in macrophages and their ligands against mycobacteria tuberculosis.Infection and immunity · 2025Review
- Baicalein inhibits mycobacterium tuberculosis-induced macrophage M1 polarization depending on the regulation of YY1/RAB10/TLR4 pathway.Journal of inflammation (London, England) · 2025Article
- ATG16L1 controls mammalian vacuolar proton ATPase.The Journal of cell biology · 2025Article
- Mycobacterium tuberculosis triggers reduced inflammatory cytokine responses and virulence in mice lacking Tax1bp1.PLoS pathogens · 2025Article
Corrections and comments
- Commented on by
- Erratum issued
Authors and funding
16 authors at 7 institutions in 2 countries.
Funding
Abstract
Whether or not autophagy has a role in defence against Mycobacterium tuberculosis infection remains unresolved. Previously, conditional knockdown of the core autophagy component ATG5 in myeloid cells was reported to confer extreme susceptibility to M. tuberculosis in mice, whereas depletion of other autophagy factors had no effect on infection. We show that doubling cre gene dosage to more robustly deplete ATG16L1 or ATG7 resulted in increased M. tuberculosis growth and host susceptibility in mice, although ATG5-depleted mice are more sensitive than ATG16L1- or ATG7-depleted mice. We imaged individual macrophages infected with M. tuberculosis and identified a shift from apoptosis to rapid necrosis in autophagy-depleted cells. This effect was dependent on phagosome permeabilization by M. tuberculosis. We monitored infected cells by electron microscopy, showing that autophagy protects the host macrophage by partially reducing mycobacterial access to the cytosol. We conclude that autophagy has an important role in defence against M. tuberculosis in mammals.
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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.