ArticleNature microbiology2018
Autophagy proteins suppress protective type I interferon signalling in response to the murine gut microbiota.
Article in Nature microbiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 1 of them a synthesis that pooled it.
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.
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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
54 citing papers in PubMed, 1 synthesis or guideline pooled it, 82 citations in OpenAlex.
- Systematic review: gastrointestinal infection and incident inflammatory bowel disease.Alimentary pharmacology & therapeutics · 2020Pooled it
- Impact of BECLIN1 haploinsufficiency on goblet cell function and susceptibility to colitis.Cell death & disease · 2026Article
- Type I and III interferons synergize with TNF to promote virally-triggered damage to the intestinal epithelium.bioRxiv : the preprint server for biology · 2026Article
- Article
- ATG16L1 WD domain and linker regulates lipid trafficking to maintain plasma membrane integrity to limit influenza virus infection.Autophagy · 2025Article
- Gene-environment interactions shape the host-microbial interface in inflammatory bowel disease.Nature immunology · 2025Review
- Inhibition of Atg7 in intestinal epithelial cells drives resistance against Citrobacter rodentium.Cell death & disease · 2025Article
- Autophagy and Bacterial infections.Autophagy reports · 2025Review
- Exploring the Connections: Autophagy, Gut Microbiota, and Inflammatory Bowel Disease Pathogenesis.Journal of inflammation research · 2024Review
- Antimicrobial overproduction sustains intestinal inflammation by inhibiting Enterococcus colonization.Cell host & microbe · 2023Article
- Type-I interferons promote innate immune tolerance in macrophages exposed to Mycobacterium ulcerans vesicles.PLoS pathogens · 2023Article
- Gut Microbiota in Autophagy Regulation: New Therapeutic Perspective in Neurodegeneration.Life (Basel, Switzerland) · 2023Review
- How autophagy, a potential therapeutic target, regulates intestinal inflammation.Frontiers in immunology · 2023Review
- Review of microbiota gut brain axis and innate immunity in inflammatory and infective diseases.Frontiers in cellular and infection microbiology · 2023Review
- Article
- OTUD7B deubiquitinates SQSTM1/p62 and promotes IRF3 degradation to regulate antiviral immunity.Autophagy · 2022Article
- Alterations of autophagic and innate immune responses by the Crohn's disease-associatedWorld journal of gastroenterology · 2022Review
- From Intestinal Epithelial Homeostasis to Colorectal Cancer: Autophagy Regulation in Cellular Stress.Antioxidants (Basel, Switzerland) · 2022Review
- Microbial byproducts determine reproductive fitness of free-living and parasitic nematodes.Cell host & microbe · 2022Article
- Intestinal antiviral signaling is controlled by autophagy geneAutophagy · 2022Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
As a conserved pathway that lies at the intersection between host defence and cellular homeostasis, autophagy serves as a rheostat for immune reactions. In particular, autophagy suppresses excess type I interferon (IFN-I) production in response to viral nucleic acids. It is unknown how this function of autophagy relates to the intestinal barrier where host-microbe interactions are pervasive and perpetual. Here, we demonstrate that mice deficient in autophagy proteins are protected from the intestinal bacterial pathogen Citrobacter rodentium in a manner dependent on IFN-I signalling and nucleic acid sensing pathways. Enhanced IFN-stimulated gene expression in intestinal tissue of autophagy-deficient mice in the absence of infection was mediated by the gut microbiota. Additionally, monocytes infiltrating into the autophagy-deficient intestinal microenvironment displayed an enhanced inflammatory profile and were necessary for protection against C. rodentium. Finally, we demonstrate that the microbiota-dependent IFN-I production that occurs in the autophagy-deficient host also protects against chemical injury of the intestine. Thus, autophagy proteins prevent a spontaneous IFN-I response to microbiota that is beneficial in the presence of infectious and non-infectious intestinal hazards. These results identify a role for autophagy proteins in controlling the magnitude of IFN-I signalling at the intestinal barrier.
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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.