Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA384377 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5482560_1.fastq.gz | Fastqsanger.gz | |||
| SRR5482560_2.fastq.gz | Fastqsanger.gz | |||
| SRR5482561_1.fastq.gz | Fastqsanger.gz | |||
| SRR5482561_2.fastq.gz | Fastqsanger.gz | |||
| SRR5482562_1.fastq.gz | Fastqsanger.gz |
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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 RORt and ROR and reduced expression of Foxp3, a transcription factor known to antagonize RORt function.
2018-02-15 | GSE98242 | GEO
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
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
Project description:The FRA1–JUNB/AP-1 transcription complex, a downstream target of STAT3, induces Th17 differentiation and promotes experimental autoimmune arthritis
| PRJNA419679 | ENA
Project description:To understand the mechanisms through which JunB regulates Tregs-mediated immune regulation, we examined the global gene expression profiles in the JunB WT and KO Tregs by performing RNA sequencing (RNA-seq) analysis.
2019-05-07 | GSE129060 | GEO
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
Project description:- transcription factor interferon regulatory factor 4 (IRF4) = crucial transcription factor for different immune cells, incl pro-inflammatory Th17 and anti-inflammatory Treg cells
- IRF4 is essential for the cell differentiation and fate determination
- however molecular mechanisms of IRF4-mediated gene expression in fully differentiated Th17/Treg cells are still not fully understood
- integration of data derived from affinity-purification and full mass spectrometry-based proteome analysis with chromatin immune precipitation sequencing (ChIP-Seq)
- characterization of proteins generally involved in the T cell development as well as subtype-specific differentiation and identification of novel, yet uncharted IRF4 interactors
2024-08-02 | PXD044298 | JPOST Repository
Project description:Cellular binary fate decisions require the progeny to silence genes associated with the alternative fate. The major subsets of alpha:beta T cells have been extensively studied as a model system for fate decisions. While the transcription factor RUNX3 is required for the initiation of Cd4 silencing in CD8 T cell progenitors, it is not required to maintain the silencing of Cd4 and other helper T lineage genes. The other runt domain containing protein, RUNX1, silences Cd4 in an earlier T cell progenitor, but this silencing is reversed whereas the gene silencing after RUNX3 expression is not reverse. Therefore, we hypothesized that RUNX3 and not RUNX1 recruits other factors that maintains the silencing of helper T lineage genes in CD8 T cells. To this end, we performed a proteomics screen of RUNX1 and RUNX3 to determine candidate silencing factors.
2019-11-12 | PXD007511 | Pride
Project description:Transcriptional mechanisms that drive angiogenesis and organotypic endothelial specialization are poorly understood. Here, we show that retinal endothelial sphingosine 1-phosphate receptors (S1PRs), which restrain vascular endothelial growth factor (VEGF)-induced angiogenesis, spatially restrict expression of JunB, a member of the activator protein 1 (AP-1) family of transcription factors. Mechanistically, VEGF induces JunB expression at the sprouting vascular front while S1PR-dependent VE-cadherin assembly suppresses JunB expression in the nascent vascular network, thus creating a gradient of this transcription factor. Endothelial-specific JunB knockout mice showed diminished expression of neurovascular guidance genes and attenuated retinal vascular network progression. In addition, endothelial S1PR signaling is required for normal expression of ß-catenin-dependent genes such as TCF/LEF1 and ZIC3 transcription factors, transporters and junctional proteins. These results show that S1PR signaling restricts JunB function to the expanding vascular front, thus creating an AP-1 transcriptional factor gradient and enables organotypic endothelial specialization of the vascular network.
2019-12-05 | GSE141440 | GEO
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.
2022-03-31 | GSE131292 | GEO