Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE98413 | GEO | 2017/06/17

SECONDARY ACCESSION(S): PRJNA385056

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Role of JunB in Th17 cell effector stability [ChIP-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 | GSE98412 | GEO

The AP-1 Transcription Factor JunB Is Required for Th17 Cell Differentiation

Project description:Interleukin (IL)-17-producing T helper (Th17) cells are crucial for host defense against extracellular microbes and pathogenesis of autoimmune diseases. Here we show that the AP-1 transcription factor JunB is required for Th17 cell development. Junb-deficient CD4+ T cells are able to develop in vitro into various helper T subsets except Th17. The RNA-seq transcriptome analysis reveals that JunB is crucial for the Th17-specific gene expression program. Junb-deficient mice are completely resistant to experimental autoimmune encephalomyelitis, a Th17-mediated inflammatory disease, and naive T helper cells from such mice fail to differentiate into Th17 cells. JunB appears to activate Th17 signature genes by forming a heterodimer with BATF, another AP-1 factor essential for Th17 differentiation. The mechanism whereby JunB controls Th17 cell development likely involves activation of the genes for the Th17 lineage-specifying orphan receptors RORt and ROR and reduced expression of Foxp3, a transcription factor known to antagonize RORt function.

2018-02-15 | GSE98242 | GEO

Role of JunB in Th17 cell effector stability

Project description:Role of JunB in Th17 cell effector stability

| PRJNA385018 | ENA

JunB is essential for IL-23-dependent pathogenicity of Th17 cells.

Project description:To understand molecular mechanisms by which JunB regulates Th17 differentiation, we performed microarray analyses of JunB-deficient and control Th17 cells.

2017-04-11 | GSE86499 | GEO

JunB is essential for IL-23-dependent pathogenicity of Th17 cells.

Project description:To understand molecular mechanisms by which JunB regulates Th17 differentiation, we performed ChIP-seq analyses of JunB-deficient and control Th17 cells.

2017-04-11 | GSE86535 | GEO

JunB regulates the common and lineage-specific transcriptional programs of distinct CD4+ effector T cells

Project description:IRF4 is critical for differentiation of various CD4+ effector T cells, such as T helper 1 (Th1), Th2, and Th17 subsets, through interaction with BATF-containing AP-1 heterodimers. A major BATF heterodimeric partner, JunB, regulates Th17 differentiation, but the role of JunB in other CD4+ effector T subsets is not fully understood. Here we demonstrate that JunB is essential for accumulation of Th1 and Th2 cells, as well as Th17 cells, both in vitro and in vivo. In mice immunized with lipopolysaccharide (LPS), papain, or complete Freund’s adjuvant (CFA), that induce predominantly Th1, Th2 and Th17 cells, respectively, accumulation of antigen-primed, Junb-deficient CD4+ T cells is significantly impaired. Loss of JunB decreases viability of cells activated under Th1-, Th2-, and Th17-polarizing conditions. RNA-sequencing (RNA-seq) and chromatin immunoprecipitation sequencing (ChIP-seq) reveal that JunB directly regulates expression of various genes that are commonly induced in priming of naïve CD4+ T cells, including a pro-apoptotic gene Bcl2l11 (encoding Bim), and genes that are specifically induced in Th1, Th2, and Th17 cells. Furthermore, JunB colocalizes with BATF and IRF4 at genomic regions for approximately half of JunB direct target genes. Taken together, JunB, in collaboration with BATF and IRF4, serves a critical function in differentiation of diverse CD4+ T cells by controlling common and lineage-specific gene expression.

2021-10-01 | GSE172490 | 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

JunB plays a crucial role in the development of regulatory T cells by increasing a sensitivity to interleukin-2

2022-03-31 | GSE131292 | GEO

Global miRNA expression profiling of Junb-deficient murine embryonic fibroblasts

Project description:The AP-1 transcription factor subunit Junb acts as a context-dependent transcriptional regulator. While positive regulatory functions of Junb are widely studied, the mechanism by which Junb exerts negative regulatory functions remains unclear. miRNAs could translate repressor functions of Junb. Therefore, the aim of this study was to identify Junb-dependent miRNAs in immortalized fibroblasts (MEFs) derived from murine Junb knock-out and wildtype embryos. Cells were published previously in Licht et al. (2010) J Clin Invest. 120(7):2307-18.

2015-10-13 | GSE43380 | GEO

JUNB ChIP-seq

Project description:JUNB ChIP-seq

| PRJNA802851 | ENA