ArticleThe Journal of experimental medicine2022
The transcription factor HIF-1α mediates plasticity of NKp46+ innate lymphoid cells in the gut.
Article in The Journal of experimental medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 46 citations in OpenAlex.
- DNA From Neutrophil Extracellular Traps Restricts Group 3 Innate Lymphoid Cells Function in Intestinal Epithelial Repair via CCDC25.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Spatial and Phenotypic Heterogeneity of ILC Subsets in Mouse Lung Under Type 2 Inflammatory Conditions.European journal of immunology · 2026Article
- Disturbed LTB4 Metabolism in ILC2s Aggravates Ulcerative Colitis via Intercellular ATP Accumulation.Inflammation · 2026Article
- The shifting balance: innate lymphoid cell plasticity in chronic gut diseases.Frontiers in immunology · 2026Review
- Type 1 innate lymphoid cell-immature neutrophil axis suppresses acute tissue inflammation.Nature communications · 2025Article
- Intestinal IL-33 promotes microbiota-derived trimethylamine N -oxide synthesis and drives metabolic dysfunction-associated steatotic liver disease progression by exerting dual regulation on HIF-1α.Hepatology (Baltimore, Md.) · 2025Article
- Review
- Exploration potential sepsis-ferroptosis mechanisms through the use of CETSA technology and network pharmacology.Scientific reports · 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
- The transcription factor HIF-1α in NKp46+ ILCs limits chronic intestinal inflammation and fibrosis.Life science alliance · 2024Article
- Group 3 innate lymphoid cells in intestinal health and disease.Nature reviews. Gastroenterology & hepatology · 2024Review
- Transcription factor Tox2 is required for metabolic adaptation and tissue residency of ILC3 in the gut.Immunity · 2024Article
- Group 1 ILCs: Heterogeneity, plasticity, and transcriptional regulation.Immunological reviews · 2024Review
- Eomes-dependent mitochondrial regulation promotes survival of pathogenic CD4+ T cells during inflammation.The Journal of experimental medicine · 2024Article
- Crosstalk between hypoxia-inducible factor-1α and short-chain fatty acids in inflammatory bowel disease: key clues toward unraveling the mystery.Frontiers in immunology · 2024Review
- mTORC2 acts as a gatekeeper for mTORC1 deficiency-mediated impairments in ILC3 development.Acta pharmacologica Sinica · 2023Article
- Resting natural killer cell homeostasis relies on tryptophan/NADEMBO reports · 2023Article
- Involvement of ILC1-like innate lymphocytes in human autoimmunity, lessons from alopecia areata.eLife · 2023Article
- Innate Lymphoid Cell Plasticity in Mucosal Infections.Microorganisms · 2023Review
Corrections and comments
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Authors and funding
14 authors at 7 institutions in 6 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gut innate lymphoid cells (ILCs) show remarkable phenotypic diversity, yet microenvironmental factors that drive this plasticity are incompletely understood. The balance between NKp46+, IL-22-producing, group 3 ILCs (ILC3s) and interferon (IFN)-γ-producing group 1 ILCs (ILC1s) contributes to gut homeostasis. The gut mucosa is characterized by physiological hypoxia, and adaptation to low oxygen is mediated by hypoxia-inducible transcription factors (HIFs). However, the impact of HIFs on ILC phenotype and gut homeostasis is not well understood. Mice lacking the HIF-1α isoform in NKp46+ ILCs show a decrease in IFN-γ-expressing, T-bet+, NKp46+ ILC1s and a concomitant increase in IL-22-expressing, RORγt+, NKp46+ ILC3s in the gut mucosa. Single-cell RNA sequencing revealed HIF-1α as a driver of ILC phenotypes, where HIF-1α promotes the ILC1 phenotype by direct up-regulation of T-bet. Loss of HIF-1α in NKp46+ cells prevents ILC3-to-ILC1 conversion, increases the expression of IL-22-inducible genes, and confers protection against intestinal damage. Taken together, our results suggest that HIF-1α shapes the ILC phenotype in the gut.
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