Rbpj expression in regulatory T cells is critical for restraining TH2 responses.
Ontology highlight
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 remi
SUBMITTER: Delacher M
PROVIDER: S-EPMC6453958 | biostudies-literature | 2019 Apr
REPOSITORIES: biostudies-literature
ACCESS DATA