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