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

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

PROVIDER: PRJNA496595 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8062090_1.fastq.gz	Fastqsanger.gz
	SRR8062090_2.fastq.gz	Fastqsanger.gz
	SRR8062091_1.fastq.gz	Fastqsanger.gz
	SRR8062091_2.fastq.gz	Fastqsanger.gz
	SRR8062092_1.fastq.gz	Fastqsanger.gz

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

Project description: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.

2018-11-19 | GSE121295 | GEO

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 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]

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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 [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 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

ChIP-Seq analysis of PU.1, BATF, and JunB in murine BMDCs

Project description:Purpose: The purpose of this study is to identify the genome-wide binding sites for IRF4 interaction partners PU.1, BATF, and JunB in dendritic cells. These ChIP-seq data were integrated with gene expression analysis in IRF4-sufficient and -deficient BMDCs in order to assemble an IRF4 gene regulatory network. Hematopoietic bone marrow progenitors from C57BL/6 mice were differentiated with GM-CSF and IL-4 for 5 days. On day 6, BMDCs were stimulated for 6 hours with 100ng/ml LPS. Fixed chromatin was immunoprecipitated with anti-PU.1, BATF, and JunB antibodies and subjected to high-throughput sequencing. The sequencing data for the input DNA was previously submitted as GSM999807.

2013-12-22 | E-GEOD-52772 | biostudies-arrayexpress

Role of JunB in Th17 cell effector stability

Project description:Role of JunB in Th17 cell effector stability

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High-dimensional single cell analysis reveals an effector Treg molecular program that correlates with lung cancer progression

Project description:Anti-tumor immune responses are counteracted by CD4+ regulatory T (Treg) cells in the tumor micronenvironment, but the molecular mechanisms responsible for the enhanced suppressive activity of Tregs are poorly defined. High-dimensional single cell profiling of millions of single CD4+ and CD8+ T cells from 53 chemotherapy-na‹ve individuals with lung adenocarcinoma identified the transcription factor IRF4 as constitutively expressed by effector CD4+ Tregs present exclusively in tumors. These IRF4+, but not the quiescent IRF4_ÿTregs expressed a vast array of suppressive molecules, positively correlated with multiple inhibitory and exhausted subpopulations of T cells and were more abundant in rapidly progressing patients. Integration of transcriptomic data and whole genome binding sites of transcription factors further revealed that IRF4, either alone or in combination with its partner BATF, directly controlled a molecular program responsible for Treg hyperproliferation and suppressive functions that included CTLA-4, ICOS, TNFRSF9 (4-1BB) and IL1R2, previously shown to impact survival in lung cancer. Thus, interfering with the IRF4-dependent molecular program may represent a novel immunotherapeutic approach capable to block immunosuppression in the tumor microenvironment without inducing autoimmunity in peripheral tissues.ÿ

2020-03-03 | GSE128822 | GEO

ChIP-Seq analysis of PU.1, BATF, and JunB in murine BMDCs

2013-12-22 | GSE52772 | GEO