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Role of JunB in Th17 cell effector stability

ABSTRACT: Role of JunB in Th17 cell effector stability

PROVIDER: PRJNA385018 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5491270.fastq.gz	Fastqsanger.gz
	SRR5491271.fastq.gz	Fastqsanger.gz
	SRR5491272.fastq.gz	Fastqsanger.gz
	SRR5491263.fastq.gz	Fastqsanger.gz
	SRR5491264.fastq.gz	Fastqsanger.gz

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Similar Datasets

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 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 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

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

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

Role of JunB in Th17 cell effector stability

Project description:This SuperSeries is composed of the SubSeries listed below.

2017-06-17 | GSE98414 | GEO

Mus musculus

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

| PRJNA385056 | ENA

Mus musculus

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

| PRJNA385017 | ENA

Decoupling the role of RORgt in the differentiation and effector function of Th17 cells

Project description:RORgt is known to instruct the differentiation of Th17 cells that mediate the pathogenesis of autoimmune diseases. However, it remains unknown whether RORgt plays a distinct role in the differentiation and effector function of Th17 cells. Here we show that mutation of RORgt lysine 256, a ubiquitination site, to arginine (K256R) separates the RORgt role in these two functions. Preventing ubiquitination at K256 via arginine substitution does not affect RORgt-dependent thymocyte development and Th17 differentiation in vitro and in vivo, however, greatly impaired the pathogenesis of Th17 cell-mediated experimental autoimmune encephalomyelitis (EAE). Mechanistically, K256R mutation impairs RORgt to bind to and activate Runx1 expression critical for Th17-mediated EAE. Thus, RORgt regulates the effector function of Th17 cells in addition to Th17 differentiation. This work informs the development of RORgt-based therapies that specifically target the effector function of Th17 cells responsible for autoimmunity.

2022-10-26 | GSE211509 | GEO

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