%0 Journal Article
%A Delacher, Michael
%A Schmidl, Christian
%A Herzig, Yonatan
%A Breloer, Minka
%A Hartmann, Wiebke
%A Brunk, Fabian
%A Kägebein, Danny
%A Träger, Ulrike
%A Hofer, Ann-Cathrin
%A Bittner, Sebastian
%A Weichenhan, Dieter
%A Imbusch, Charles D
%A Hotz-Wagenblatt, Agnes
%A Hielscher, Thomas
%A Breiling, Achim
%A Federico, Giuseppina
%A Gröne, Hermann-Josef
%A Schmid, Roland M
%A Rehli, Michael
%A Abramson, Jakub
%A Feuerer, Markus
%T Rbpj expression in regulatory T cells is critical for restraining TH2 responses.
%J Nature Communications
%V 10
%N 1
%@ 2041-1723
%C [London]
%I Nature Publishing Group UK
%M DKFZ-2019-01092
%P 1621
%D 2019
%X The transcriptional regulator Rbpj is involved in T-helper (TH) subset polarization, but its function in Treg cells remains unclear. Here we show that Treg-specific Rbpj deletion leads to splenomegaly and lymphadenopathy despite increased numbers of Treg cells with a polyclonal TCR repertoire. A specific defect of Rbpj-deficient Treg cells in controlling TH2 polarization and B cell responses is observed, leading to the spontaneous formation of germinal centers and a TH2-associated immunoglobulin class switch. The observed phenotype is environment-dependent and can be induced by infection with parasitic nematodes. Rbpj-deficient Treg cells adopt open chromatin landscapes and gene expression profiles reminiscent of tissue-derived TH2-polarized Treg cells, with a prevailing signature of the transcription factor Gata-3. Taken together, our study suggests that Treg cells require Rbpj to specifically restrain TH2 responses, including their own excessive TH2-like differentiation potential.
%F PUB:(DE-HGF)16
%9 Journal Article
%$ pmid:30962454
%2 pmc:PMC6453958
%R 10.1038/s41467-019-09276-w
%U https://inrepo02.dkfz.de/record/143508