{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Krzywinska E"],"funding":["Swiss National Fund","Swiss National Centre for Competence in Research “Kidney.CH”","University of Zurich","Swiss Cancer League"],"pagination":["e20210909"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8763886"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["219(2)"],"pubmed_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 "],"journal":["The Journal of experimental medicine"],"pubmed_title":["The transcription factor HIF-1α mediates plasticity of NKp46+ innate lymphoid cells in the gut."],"pmcid":["PMC8763886"],"funding_grant_id":["KFS-4398-02-2018","KFS-5402-08-2021","N-403-06-26 HCP","310030_179235"],"pubmed_authors":["Nagarajan S","Krzywinska E","Fandrey J","Gotthardt D","Kerdiles YM","Zacharjasz J","Tambuwala MM","Peyssonnaux C","Cummins E","Sexl V","Taylor CT","Sobecki M","Pelletier A","Stockmann C"],"additional_accession":[]},"is_claimable":false,"name":"The transcription factor HIF-1α mediates plasticity of NKp46+ innate lymphoid cells in the gut.","description":"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 ","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Feb","modification":"2025-04-05T09:00:37.128Z","creation":"2025-04-05T09:00:37.128Z"},"accession":"S-EPMC8763886","cross_references":{"pubmed":["35024767"],"doi":["10.1084/jem.20210909"]}}