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| 001 | 143508 | ||
| 005 | 20240229112555.0 | ||
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| 100 | 1 | _ | |a Delacher, Michael |0 P:(DE-He78)a4340add02b610f9dbdba2dc909cbd09 |b 0 |e First author |
| 245 | _ | _ | |a Rbpj expression in regulatory T cells is critical for restraining TH2 responses. |
| 260 | _ | _ | |a [London] |c 2019 |b Nature Publishing Group UK |
| 336 | 7 | _ | |a article |2 DRIVER |
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| 520 | _ | _ | |a 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. |
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| 700 | 1 | _ | |a Hartmann, Wiebke |b 4 |
| 700 | 1 | _ | |a Brunk, Fabian |0 P:(DE-He78)79264e5eb093c3b6fe517e4ca29da19b |b 5 |
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| 700 | 1 | _ | |a Schmid, Roland M |b 17 |
| 700 | 1 | _ | |a Rehli, Michael |0 0000-0003-3992-932X |b 18 |
| 700 | 1 | _ | |a Abramson, Jakub |b 19 |
| 700 | 1 | _ | |a Feuerer, Markus |0 P:(DE-He78)f0638edf1d3f61c0d7ebb587f511733f |b 20 |e Last author |
| 773 | _ | _ | |a 10.1038/s41467-019-09276-w |g Vol. 10, no. 1, p. 1621 |0 PERI:(DE-600)2553671-0 |n 1 |p 1621 |t Nature Communications |v 10 |y 2019 |x 2041-1723 |
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