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| Home > Publications database > Rbpj expression in regulatory T cells is critical for restraining TH2 responses. |
| Home > Publications database > Rbpj expression in regulatory T cells is critical for restraining TH2 responses. |
| Journal Article | DKFZ-2019-01092 |
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2019
Nature Publishing Group UK
[London]
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Please use a persistent id in citations: doi:10.1038/s41467-019-09276-w
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.
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