ArticleMucosal immunology2021
Hypoxia enhances ILC3 responses through HIF-1α-dependent mechanism.
Article in Mucosal immunology, 2021. 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 46 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.
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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.
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Who cites it
46 citing papers in PubMed, 62 citations in OpenAlex.
- Gut microbiota and immunometabolism in obesity.Gut microbes · 2026Review
- Oxygen homeostasis: new insight of gut microbiota-host interactions.NPJ biofilms and microbiomes · 2026Review
- mtROS-NF-κB signaling supports ILC3 function and survival during sepsis-induced intestinal injury.Frontiers in immunology · 2026Article
- ILC plasticity in intestinal immune barrier remodeling: current evidence and therapeutic implications for inflammatory bowel disease.Frontiers in immunology · 2026Review
- Endothelial cell-ILC3 crosstalk via the ET-1/EDNRA axis promotes NKp46Cellular & molecular immunology · 2025Article
- Cellular Cosmetics: How Innate Lymphoid Cells Can Recontour the Tumour Microenvironment.European journal of immunology · 2025Review
- Gut Microbiota-Derived Hyocholic Acid Enhances Type 3 Immunity and Protects Against Salmonella enterica Serovar Typhimurium in Neonatal Rats.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Recent advances in non-alcoholic steatohepatitis-associated hepatocellular carcinoma: immune cells, metabolic dysregulation, and therapeutic strategies.Frontiers in oncology · 2025Review
- Intestinal oxygen utilisation and cellular adaptation during intestinal ischaemia-reperfusion injury.Clinical and translational medicine · 2025Review
- LKB1 regulates ILC3 postnatal development and effector function through metabolic programming.Frontiers in immunology · 2025Article
- Innate Lymphoid Cells.Advances in experimental medicine and biology · 2025Review
- Deciphering the Role of Innate Lymphoid Cells Group 3 in the Gut Microenvironment: A Narrative Review of Their Novel Contributions to Autoimmune Disease Pathogenesis.Journal of inflammation research · 2025Review
- Type 3 immune response protects againstEmerging microbes & infections · 2024Article
- Approaches to investigate tissue-resident innate lymphocytes metabolism at the single-cell level.Nature communications · 2024Review
- Metabolic regulation of the immune system in health and diseases: mechanisms and interventions.Signal transduction and targeted therapy · 2024Review
- Clostridioides difficile toxin B subverts germinal center and antibody recall responses by stimulating a drug-treatable CXCR4-dependent mechanism.Cell reports · 2024Article
- Transcription factor Tox2 is required for metabolic adaptation and tissue residency of ILC3 in the gut.Immunity · 2024Article
- The IRE1α/XBP1 pathway sustains cytokine responses of group 3 innate lymphoid cells in inflammatory bowel disease.The Journal of clinical investigation · 2024Article
- Group 1 ILCs: Heterogeneity, plasticity, and transcriptional regulation.Immunological reviews · 2024Review
- Targeting hypoxia-inducible factor-1 alpha suppressesGut microbes · 2023Article
Corrections and comments
- Erratum issued
Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
Group 3 innate lymphoid cells (ILC3) have a prominent role in the maintenance of intestine mucosa homeostasis. The hypoxia-inducible factor (HIF) is an important modulator of immune cell activation and a key mechanism for cellular adaptation to oxygen deprivation. However, its role on ILC3 is not well known. In this study, we investigated how a hypoxic environment modulates ILC3 response and the subsequent participation of HIF-1 signaling in this process. We found increased proliferation and activation of intestinal ILC3 at low oxygen levels, a response that was phenocopied when HIF-1α was chemically stabilized and was reversed when HIF-1 was blocked. The increased activation of ILC3 relied on a HIF-1α-dependent transcriptional program, but not on mTOR-signaling or a switch to glycolysis. HIF-1α deficiency in RORyt compartment resulted in impaired IL-17 and IL-22 production by ILC3 in vivo, which reflected in a lower expression of their target genes in the intestinal epithelium and an increased susceptibility to Clostridiodes difficile infection. Taken together, our results show that HIF-1α activation in intestinal ILC3 is relevant for their functions in steady state and infectious conditions.
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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 Socratic graph.