Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

JunB modulates an IRF4-dependent transcriptional program to regulate homeostasis and suppressive functions of effector regulatory T cells

ABSTRACT: To understand molecular mechanisms by which JunB regulates Treg function, we performed RNA-seq and ChIP-seq analyses of JunB-deficient and control Treg cells (CD4+ CD25hi). This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE121295 | GEO | 2018/11/19

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

JunB modulates an IRF4-dependent transcriptional program to regulate homeostasis and suppressive functions of effector regulatory T cells [RNA-Seq]

Project description:To understand molecular mechanisms by which JunB regulates Treg function, we performed RNA-seq analysis of JunB-deficient and control Treg cells (CD4+ CD25hi).

2018-11-19 | GSE121293 | GEO

JunB modulates an IRF4-dependent transcriptional program to regulate homeostasis and suppressive functions of effector regulatory T cells [ChIP-Seq]

Project description:To understand molecular mechanisms by which JunB regulates Treg function, we performed ChIP-seq analysis of JunB-deficient and control Treg cells (CD4+ CD25hi).

2018-11-19 | GSE121294 | GEO

JunB modulates an IRF4-dependent transcriptional program to regulate homeostasis and suppressive functions of effector regulatory T cells

Project description:JunB modulates an IRF4-dependent transcriptional program to regulate homeostasis and suppressive functions of effector regulatory T cells

| PRJNA496595 | ENA

Role of JunB in Th17 cell effector stability [RNA-seq]

Project description:Here we identify the activator protein-1 (AP-1) factor JunB as an essential regulator of Th17 cell identity. JunB activates the expression of Th17 lineage-specifying genes, and coordinately represses genes controlling Th1 and Treg fate. Through regulatory analysis, we find that JunB is a core regulator of global transcriptional programs that promote Th17 cell identity and restrict alternative CD4+ T cell potential.

2017-06-17 | GSE98413 | GEO

Role of JunB in Th17 cell effector stability [ChIP-seq]

2017-06-17 | GSE98412 | GEO

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

Project description: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.

| S-EPMC6297218 | biostudies-literature

JunB modulates an IRF4-dependent transcriptional program to regulate homeostasis and suppressive functions of effector regulatory T cells [ChIP-Seq]

Project description:JunB modulates an IRF4-dependent transcriptional program to regulate homeostasis and suppressive functions of effector regulatory T cells [ChIP-Seq]

| PRJNA496598 | ENA

JunB modulates an IRF4-dependent transcriptional program to regulate homeostasis and suppressive functions of effector regulatory T cells [RNA-Seq]

Project description:JunB modulates an IRF4-dependent transcriptional program to regulate homeostasis and suppressive functions of effector regulatory T cells [RNA-Seq]

| PRJNA496597 | ENA

JunB-dependent expression in colonic and Peyer's patch regulatory T cells

Project description:Foxp3-expressing regulatory T (Treg) cells are critical mediators of immunological tolerance to both self and microbial antigens. Tregs activate context-dependent transcriptional programs to adapt effector function to specific tissues; however, the factors controlling tissue-specific gene expression in Tregs remain unclear. Here, we find that the AP-1 transcription factor JunB regulates the intestinal adaptation of Tregs by controlling select gene expression programs in multiple Treg subsets. Treg-specific ablation of JunB results in immune dysregulation characterized by enhanced colonic T helper cell accumulation and cytokine production. However, in contrast to its classical binding-partner BATF, JunB is dispensable for maintenance of effector Tregs as well as most specialized Treg subsets. In the Peyer’s patches, JunB activates a transcriptional program facilitating the maintenance of CD25- Tregs, leading to the complete loss of T follicular regulatory cells in the absence of JunB. This defect is compounded by loss of a separate effector program found in both major colonic Treg subsets that includes the cytolytic effector molecule granzyme B. Therefore, JunB is an essential regulator of intestinal Treg effector function through pleiotropic effects on gene expression.

2020-02-26 | GSE145888 | GEO

JunB plays a crucial role in the development of regulatory T cells by regulating interleukin-2 signaling

Project description:The AP-1 transcription factor JunB is crucial for multiple biological processes, such as placental development and bone homeostasis. We recently reported that JunB plays an essential role in development of Th17 cells, and thus Junb-deficient mice are resistant to experimental autoimmune encephalomyelitis. However, the role of JunB in CD4+ T cells under other inflammatory disease conditions is unknown. Here we show that mice lacking JunB in CD4+ T cells (Junbfl/flCd4-Cre mice) were more susceptible to dextran sulfate sodium (DSS)-induced colitis, a disease model induced by innate immune cells. While the Th17-associated genes Il17a and Il22 are shown to be protective against DSS-induced colitis, their expression was not impaired in the colon of Junbfl/flCd4-Cre mice. In addition to the defect in Th17 development, the colon of Junbfl/flCd4-Cre mice exhibited reduction in regulatory T (Treg) cells. Junb-deficient CD4+ T cells needed high concentration of IL-2 for differentiating into Treg cells in vitro because of their hyporesponsiveness to IL-2. Mechanistically, JunB directly up-regulated expression of CD25, the α−chain of high affinity IL-2 receptor, thereby increasing a sensitivity to IL-2 under Treg-inducing conditions. We uncover a crucial role for JunB in development of Treg cells and defense against an epithelial cell damage-induced colitis.

2020-03-31 | GSE120814 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data