{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Delacher M"],"funding":["European Research Council"],"pagination":["1621"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6453958"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["10(1)"],"pubmed_abstract":["The transcriptional regulator Rbpj is involved in T-helper (T<sub>H</sub>) subset polarization, but its function in T<sub>reg</sub> cells remains unclear. Here we show that T<sub>reg</sub>-specific Rbpj deletion leads to splenomegaly and lymphadenopathy despite increased numbers of T<sub>reg</sub> cells with a polyclonal TCR repertoire. A specific defect of Rbpj-deficient T<sub>reg</sub> cells in controlling T<sub>H</sub>2 polarization and B cell responses is observed, leading to the spontaneous formation of germinal centers and a T<sub>H</sub>2-associated immunoglobulin class switch. The observed phenotype is environment-dependent and can be induced by infection with parasitic nematodes. Rbpj-deficient T<sub>reg</sub> cells adopt open chromatin landscapes and gene expression profiles remi"],"journal":["Nature communications"],"pubmed_title":["Rbpj expression in regulatory T cells is critical for restraining T<sub>H</sub>2 responses."],"pmcid":["PMC6453958"],"funding_grant_id":["648145"],"pubmed_authors":["Brunk F","Imbusch CD","Delacher M","Hielscher T","Breloer M","Bittner S","Herzig Y","Grone HJ","Feuerer M","Hotz-Wagenblatt A","Schmid RM","Trager U","Hofer AC","Weichenhan D","Federico G","Rehli M","Schmidl C","Kagebein D","Abramson J","Hartmann W","Breiling A"],"additional_accession":[]},"is_claimable":false,"name":"Rbpj expression in regulatory T cells is critical for restraining T<sub>H</sub>2 responses.","description":"The transcriptional regulator Rbpj is involved in T-helper (T<sub>H</sub>) subset polarization, but its function in T<sub>reg</sub> cells remains unclear. Here we show that T<sub>reg</sub>-specific Rbpj deletion leads to splenomegaly and lymphadenopathy despite increased numbers of T<sub>reg</sub> cells with a polyclonal TCR repertoire. A specific defect of Rbpj-deficient T<sub>reg</sub> cells in controlling T<sub>H</sub>2 polarization and B cell responses is observed, leading to the spontaneous formation of germinal centers and a T<sub>H</sub>2-associated immunoglobulin class switch. The observed phenotype is environment-dependent and can be induced by infection with parasitic nematodes. Rbpj-deficient T<sub>reg</sub> cells adopt open chromatin landscapes and gene expression profiles remi","dates":{"release":"2019-01-01T00:00:00Z","publication":"2019 Apr","modification":"2026-05-04T09:52:25.286Z","creation":"2025-05-18T11:07:37.887Z"},"accession":"S-EPMC6453958","cross_references":{"pubmed":["30962454"],"doi":["10.1038/s41467-019-09276-w"]}}