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IRF4/BATF and interleukin-33 orchestrate development and maintenance of adipose tissue resident regulatory T cells

ABSTRACT: To understand the differentiation of effector Tregs in more detail, we have performed transcriptional profiling of central Tregs and effector Tregs, based on Blimp1 expression. We performed RNA-sequencing of Foxp3+ regulatory T cells, comparing Blimp1/GFP+ and Blimp1/GFP- cells

ORGANISM(S): Mus musculus

PROVIDER: GSE62535 | GEO | 2014/12/11

SECONDARY ACCESSION(S): PRJNA264362

REPOSITORIES: GEO

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IRF4/BATF and interleukin-33 orchestrate development and maintenance of adipose tissue resident regulatory T cells

Project description:To understand the differentiation of effector Tregs in more detail, we have performed transcriptional profiling of central Tregs and effector Tregs, based on Blimp1 expression. We performed RNA-sequencing of Foxp3+ regulatory T cells, comparing Blimp1/GFP+ and Blimp1/GFP- cells Three biologically independent samples for each condition were sequenced (condition 1: CD4+ CD25high Blimp1/GFP+; condition 2: CD4+ CD25high Blimp1/GFP-); cells were sorted from pooled spleens and lymphnodes of Blimp1/GFP reporter mice

2014-12-11 | E-GEOD-62535 | biostudies-arrayexpress

RNA-seq analysis of transcriptomes of IL35-Treg cells and the Blimp1-Treg cells

Project description:To gain in depth transcriptional information about the two subsets of effector Tregs, we performed RNA-seq analysis to compare the transcriptomes of Thy1.1+Blimp1- (Ebi3-Tregs) and Thy1.1-Blimp1+ (Blimp1-Tregs) Tregs. We found ~173 unique genes with differential expression between the two effector subsets.

2019-08-31 | GSE103456 | GEO

BATF-JUN is critical for IRF4-mediated transcription in T cells.

Project description: Not available

| S-EPMC3537508 | biostudies-literature

Genome-wide profiling of muscle Treg cells from IL-33 treated mice

Project description:We report gene expression of Treg cells isolated from injured muscle in IL-33 vs PBS treated mice. Male Foxp3-GFP C57BL/6 reporter (2 months old) mice were injured intramuscularly with cardiotoxin/rIL-33 (0.3 ug/muscle). Tregs were sorted directly into Trizol from injured muscle 4 days post-injury. Gene expression profiling of muscle Tregs from IL-33 vs PBS injured mice.

2016-01-12 | E-GEOD-76722 | biostudies-arrayexpress

BLIMP1 induces cancer immune evasion by modulating the USP22-SPI1-PD-L1 axis in hepatocellular carcinoma cells

Project description:To clarify the potential BLIMP1 downstream target regulating PD-L1 expression, we performed proteomics analysis using BLIMP1 Hep3B cells and control cells. Proteomics analysis revealed that SPI1 may serve as a pivotal transcriptional factor that enhances PD-L1 expression by acting as a downstream effector of BLIMP1.

2022-11-23 | PXD037621 | Pride

ChIP-Seq analysis of BATF, IRF4, the Jun proteins, and histone modifications in effector CD8+ T cells

Project description:The transcription factor BATF is required for Th17 and TFH differentiation. Here, we show that BATF also has a fundamental role in regulating effector CD8+ T cell differentiation. BATF-deficient CD8+ T cells show profound defects in effector expansion and undergo proliferative and metabolic catastrophe early after antigen encounter. BATF, together with IRF4 and Jun proteins, binds to and promotes early expression of genes encoding lineage-specific transcription-factors (T-bet and Blimp-1) and cytokine receptors, while paradoxically repressing genes encoding effector molecules (IFNg and granzyme B). Thus, BATF amplifies TCR-dependent transcription factor expression and augments inflammatory signal propagation but restrains effector gene expression. This checkpoint prevents irreversible commitment to an effector fate until a critical threshold of downstream transcriptional activity has been achieved. This is an examination of 5 different transcription factors (TFs) with 5 different histone modifications in effector CD8+ T cells. Two of the TFs (BATF and IRF4) and the histone modifications were replicated. Appropriate control sequence files for ChIP input, IgG ChIP, and Total H3 are also included.

2014-03-02 | E-GEOD-54191 | biostudies-arrayexpress

IL-33 signaling alters regulatory T cell diversity in support of tumor development

Project description:Regulatory T cells (Tregs) can impair anti-tumor immune responses and are associated with poor prognosis in multiple cancer types. Tregs in human tumors span diverse transcriptional states distinct from those of peripheral Tregs, but their contribution to tumor development remains unknown. Here, we use single cell RNA-Seq to longitudinally profile dynamic shifts in the distribution of Tregs in a genetically-engineered mouse model of lung adenocarcinoma. In this model, interferon-responsive Tregs are more prevalent early in tumor development, while a specialized effector phenotype characterized by enhanced expression of the interleukin 33 receptor ST2 is predominant in advanced disease. Treg-specific deletion of ST2 alters the evolution of effector Treg diversity, increases infiltration of CD8+ T cells into tumors, and decreases tumor burden. Our study shows that ST2 plays a critical role in Treg-mediated immunosuppression in cancer, highlighting potential paths for therapeutic intervention.

2019-12-03 | GSE140431 | GEO

IL-33 signaling alters regulatory T cell diversity in support of tumor development

2019-12-03 | GSE129914 | GEO

TIGIT+ Tregs

Project description:TIGIT+ Tregs suppress Th1 and Th17 responses while sparing Th2 responses. Analysis of global gene expression of TIGIT+ vs. TIGIT- Tregs from naive mice reveled that TIGIT+ Tregs display an activated phenotype and are enriched for Treg signature genes including the Treg effector molecule Fgl2 which enables them to selectively spare Th2 responses. TIGIT+ and TIGIT- Tregs were sorted from naïve Foxp3-GFP KI mice (pooled spleen and lymph nodes) TIGIT: T cell immunoreceptor with Ig and ITIM domains

2014-12-12 | E-GEOD-56299 | biostudies-arrayexpress

IL-33 signaling alters regulatory T cell diversity in support of tumor development [2018]

2019-12-03 | GSE139229 | GEO

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