{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Stehle C"],"funding":["Deutsche Forschungsgemeinschaft","The state of Berlin and the “European Regional Development Fund”","Dr. Rolf M. Schwiete Foundation","Leibniz-Gemeinschaft","Wellcome Trust"],"pagination":["1231-1244"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7614953"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["22(10)"],"pubmed_abstract":["The generation of lymphoid tissues during embryogenesis relies on group 3 innate lymphoid cells (ILC3) displaying lymphoid tissue inducer (LTi) activity and expressing the master transcription factor RORγt. Accordingly, RORγt-deficient mice lack ILC3 and lymphoid structures, including lymph nodes (LN). Whereas T-bet affects differentiation and functions of ILC3 postnatally, the role of T-bet in regulating fetal ILC3 and LN formation remains completely unknown. Using multiple mouse models and single-cell analyses of fetal ILCs and ILC progenitors (ILCP), here we identify a key role for T-bet during embryogenesis and show that its deficiency rescues LN formation in RORγt-deficient mice. Mechanistically, T-bet deletion skews the differentiation fate of fetal ILCs and promotes the accumulation"],"journal":["Nature immunology"],"pubmed_title":["T-bet and RORα control lymph node formation by regulating embryonic innate lymphoid cell differentiation."],"pmcid":["PMC7614953"],"funding_grant_id":["TRR130, TP17","INST 335/597-1 FUGG","RO3565/2-1","RO3565/1-1","TRR241 B02","110199","110199/Z/15/Z","K259/2019","DFG-SFB TRR241 B03","SPP1937 (HA5354/8-1 and 8-2)"],"pubmed_authors":["Withers DR","Mashreghi MF","Finke D","Romagnani C","Ruckert T","Hauser AE","Zimmermann J","Durek P","Gajdasik DW","Fiancette R","Stehle C","Ulbricht C","Willis C","Chang HD"],"additional_accession":[]},"is_claimable":false,"name":"T-bet and RORα control lymph node formation by regulating embryonic innate lymphoid cell differentiation.","description":"The generation of lymphoid tissues during embryogenesis relies on group 3 innate lymphoid cells (ILC3) displaying lymphoid tissue inducer (LTi) activity and expressing the master transcription factor RORγt. Accordingly, RORγt-deficient mice lack ILC3 and lymphoid structures, including lymph nodes (LN). Whereas T-bet affects differentiation and functions of ILC3 postnatally, the role of T-bet in regulating fetal ILC3 and LN formation remains completely unknown. Using multiple mouse models and single-cell analyses of fetal ILCs and ILC progenitors (ILCP), here we identify a key role for T-bet during embryogenesis and show that its deficiency rescues LN formation in RORγt-deficient mice. Mechanistically, T-bet deletion skews the differentiation fate of fetal ILCs and promotes the accumulation","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Oct","modification":"2025-04-18T22:31:35.202Z","creation":"2025-04-07T10:13:56.122Z"},"accession":"S-EPMC7614953","cross_references":{"pubmed":["34556887"],"doi":["10.1038/s41590-021-01029-6"]}}