Rbpj expression in regulatory T cells is critical for restraining TH2 responses. View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2019-12

AUTHORS

Michael Delacher, Christian Schmidl, Yonatan Herzig, Minka Breloer, Wiebke Hartmann, Fabian Brunk, Danny Kägebein, Ulrike Träger, Ann-Cathrin Hofer, Sebastian Bittner, Dieter Weichenhan, Charles D Imbusch, Agnes Hotz-Wagenblatt, Thomas Hielscher, Achim Breiling, Giuseppina Federico, Hermann-Josef Gröne, Roland M Schmid, Michael Rehli, Jakub Abramson, Markus Feuerer

ABSTRACT

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. More... »

PAGES

1621

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/s41467-019-09276-w

    DOI

    http://dx.doi.org/10.1038/s41467-019-09276-w

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1113300676

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/30962454


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