Unknown

Dataset Information

0

JunB regulates homeostasis and suppressive functions of effector regulatory T cells.


ABSTRACT: Foxp3-expressing CD4+ regulatory T (Treg) cells need to differentiate into effector Treg (eTreg) cells to maintain immune homeostasis. T-cell receptor (TCR)-dependent induction of the transcription factor IRF4 is essential for eTreg differentiation, but how IRF4 activity is regulated in Treg cells is still unclear. Here we show that the AP-1 transcription factor, JunB, is expressed in eTreg cells and promotes an IRF4-dependent transcription program. Mice lacking JunB in Treg cells develop multi-organ autoimmunity, concomitant with aberrant activation of T helper cells. JunB promotes expression of Treg effector molecules, such as ICOS and CTLA4, in BATF-dependent and BATF-independent manners, and is also required for homeostasis and suppressive functions of eTreg. Mechanistically, JunB facilitates the accumulation of IRF4 at a subset of IRF4 target sites, including those located near Icos and Ctla4. Thus, JunB is a critical regulator of IRF4-dependent Treg effector programs, highlighting important functions for AP-1 in Treg-mediated immune homeostasis.

SUBMITTER: Koizumi SI 

PROVIDER: S-EPMC6297218 | BioStudies | 2018-01-01

REPOSITORIES: biostudies

Similar Datasets

2020-01-01 | S-EPMC6959360 | BioStudies
2018-01-01 | S-EPMC5974344 | BioStudies
2020-01-01 | S-EPMC7137613 | BioStudies
1000-01-01 | S-EPMC5869772 | BioStudies
2018-11-19 | GSE121294 | GEO
2018-11-19 | GSE121295 | GEO
2019-01-01 | S-EPMC6761015 | BioStudies
2019-01-01 | S-EPMC6410771 | BioStudies
2019-11-07 | GSE126806 | GEO
2019-11-07 | GSE126800 | GEO