Rbpj expression in regulatory T cells is critical for restraining TH2 responses

Delacher M, Schmidl C, Herzig Y, Breloer M, Hartmann W, Brunk F, Kaegebein D, Traeger U, Hofer AC, Bittner S, Weichenhan D, Imbusch CD, Hotz-Wagenblatt A, Hielscher T, Breiling A, Federico G, Groene HJ, Schmid RM, Rehli M, Abramson J, Feuerer M (2019)


Publication Type: Journal article

Publication year: 2019

Journal

Book Volume: 10

Article Number: 1621

Journal Issue: 1

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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How to cite

APA:

Delacher, M., Schmidl, C., Herzig, Y., Breloer, M., Hartmann, W., Brunk, F.,... Feuerer, M. (2019). Rbpj expression in regulatory T cells is critical for restraining TH2 responses. Nature Communications, 10(1). https://doi.org/10.1038/s41467-019-09276-w

MLA:

Delacher, Michael, et al. "Rbpj expression in regulatory T cells is critical for restraining TH2 responses." Nature Communications 10.1 (2019).

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