{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Li Q"],"funding":["NCRR NIH HHS","NIAID NIH HHS","NIH","Tsinghua-Peking Center for Life Sciences"],"pagination":["258-270.e5"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC5828523"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["48(2)"],"pubmed_abstract":["Group 2 innate lymphoid cells (ILC2s) are a specialized subset of lymphoid effector cells that are critically involved in allergic responses; however, the mechanisms of their regulation remain unclear. We report that conditional deletion of the E3 ubiquitin ligase VHL in innate lymphoid progenitors minimally affected early-stage bone marrow ILC2s but caused a selective and intrinsic decrease in mature ILC2 numbers in peripheral non-lymphoid tissues, resulting in reduced type 2 immune responses. VHL deficiency caused the accumulation of hypoxia-inducible factor 1α (HIF1α) and attenuated interleukin-33 (IL-33) receptor ST2 expression, which was rectified by HIF1α ablation or inhibition. HIF1α-driven expression of the glycolytic enzyme pyruvate kinase M2 downmodulated ST2 expression via epige"],"journal":["Immunity"],"pubmed_title":["E3 Ligase VHL Promotes Group 2 Innate Lymphoid Cell Maturation and Function via Glycolysis Inhibition and Induction of Interleukin-33 Receptor."],"pmcid":["PMC5828523"],"funding_grant_id":["RO1AI123398","NSFC81630041","YFA0505802","S10 RR027366","R01 AI123398","YFC0903900"],"pubmed_authors":["Zhang W","Wan Q","Zou L","Elly C","Li D","Zheng M","Zhang X","Li Q","Lee JH","Liu YC"],"additional_accession":[]},"is_claimable":false,"name":"E3 Ligase VHL Promotes Group 2 Innate Lymphoid Cell Maturation and Function via Glycolysis Inhibition and Induction of Interleukin-33 Receptor.","description":"Group 2 innate lymphoid cells (ILC2s) are a specialized subset of lymphoid effector cells that are critically involved in allergic responses; however, the mechanisms of their regulation remain unclear. We report that conditional deletion of the E3 ubiquitin ligase VHL in innate lymphoid progenitors minimally affected early-stage bone marrow ILC2s but caused a selective and intrinsic decrease in mature ILC2 numbers in peripheral non-lymphoid tissues, resulting in reduced type 2 immune responses. VHL deficiency caused the accumulation of hypoxia-inducible factor 1α (HIF1α) and attenuated interleukin-33 (IL-33) receptor ST2 expression, which was rectified by HIF1α ablation or inhibition. HIF1α-driven expression of the glycolytic enzyme pyruvate kinase M2 downmodulated ST2 expression via epige","dates":{"release":"2018-01-01T00:00:00Z","publication":"2018 Feb","modification":"2026-04-29T16:30:36.123Z","creation":"2019-03-26T22:55:00Z"},"accession":"S-EPMC5828523","cross_references":{"pubmed":["29452935"],"doi":["10.1016/j.immuni.2017.12.013"]}}