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Whole-transcriptome quantitative analysis of WT versus Ikzf4-/- CD4+ T cells cultured in Th1-polarizing conditions

ABSTRACT: Whole-transcriptome quantitative analysis of WT versus Ikzf4-/- CD4+ T cells cultured in Th1-polarizing conditions

PROVIDER: PRJNA614538 | ENA |

REPOSITORIES: ENA

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Whole-transcriptome quantitative analysis of WT versus Ikzf4-/- CD4+ T cells cultured in Th1-polarizing conditions

Project description:Purpose: To evaluate transcriptome-wide alterations in CD4+ T cells cultured under Th1-polarizing conditions in the absence of the Ikaros zinc finger transcription factor Eos via RNA-seq analysis.

2020-03-24 | GSE147428 | GEO

Effect of SGC0946 and SGC0649 on CD4+ T cells under Th1 polarizing conditions

Project description:Comparison between naïve CD4+ mouse T cells and either bona fide IFNg+ and IFNg- CD4+ T cells after culturing under Th1 polarizing conditions in the presence of either the epigenetic probe SGC0946 or SGC0649

2018-08-20 | GSE106978 | GEO

Whole-transcriptome quantitative analysis of WT versus Ikzf3-/- CD4+ T cells cultured in Th1-polarizing or Tfh-polarizing conditions

Project description:Effective immunity to viruses such as influenza and SARS-CoV-2 requires the generation of CD4+ T cell subsets that coordinate complementary aspects of the immune response. These include T follicular helper (TFH) and T helper 1 (TH1) cells, which promote humoral and cell-mediated helper responses, respectively. A third population, CD4+ cytotoxic T lymphocytes (CD4-CTLs) facilitates clearance of infection via mechanisms normally associated with CD8+ T cells, including perforin-mediated destruction of infected cells. Here, we identify the transcription factor Aiolos as a reciprocal regulator of TFH and CD4-CTL responses. We demonstrate that Aiolos deficiency compromises TFH differentiation and antibody production during influenza infection. Conversely, we find that CD4+ T cells acquire a cytotoxic-like program in the absence of Aiolos, including increased expression of the CTL-associated transcription factors Eomes and Blimp-1. We further show that while Aiolos positively regulates the TFH transcriptional regulators Zfp831, Tcf-1 and Bcl-6, it also directly represses expression of IL-2Ra and IL-2/STAT5-driven expression of the cytotoxic gene program. Thus, our findings identify Aiolos as a pivotal regulator of TFH and CD4-CTL differentiation and highlight its potential as a therapeutic target for the manipulation of CD4+ T cell humoral and cytotoxic responses.

2023-02-01 | GSE203065 | GEO

ATAC-seq analysis of WT versus Ikzf3-/- CD4+ T cells cultured in Th1-polarizing or Tfh-polarizing conditions

2023-02-01 | GSE203064 | GEO

WT versus Ikzf3-/- CD4+ T cells cultured in Th1-polarizing or Tfh-polarizing conditions

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

2023-02-01 | GSE203066 | GEO

Effect of SGC0946 and SGC0649 on CD4+ T cells under Th1 polarizing conditions

Project description:Effect of SGC0946 and SGC0649 on CD4+ T cells under Th1 polarizing conditions

| PRJNA418714 | ENA

Transcriptomic analysis of WT versus Ikzf4-/- CD4+ T cells cultured in Th2-polarizing conditions

Project description:The Ikaros zinc finger transcription factor Eos has been commonly implicated in regulatory T cells to promote their immunosuppressive functions. Paradoxically, a new role is emerging for Eos in promoting pro-inflammatory responses of conventional CD4+ T cells in the dysregulated setting of autoimmunity. Even so, the precise role of Eos in regulating the differentiation and function of healthy effector CD4+ T cell subsets remains unclear. Here, we find that Eos is a positive regulator of CD4+ T helper 2 (TH2) cells—effector T cells implicated in the induction of allergic asthma. Using murine in vitro TH2 cells and an in vivo house dust mite asthma model, we found that Eos-deficient T cells had reduced expression of key TH2 transcription factors, effector cytokines, and differentiation receptors. Mechanistically, among various TH2-polarizing pathways, the IL-2/STAT5 axis and its downstream TH2 gene targets emerged as one of the most significantly downregulated networks in Eos deficiency. Using in vitro TH2 cells and overexpression of Eos zinc-finger-domain mutants, we discovered that Eos forms a novel complex with and supports the tyrosine-phosphorylated signaling activity of STAT5. Overall, these data define a novel regulatory mechanism whereby Eos promotes IL-2/STAT5 activity to facilitate TH2 differentiation.

2023-02-01 | GSE216737 | GEO

Gene expression analysis of Akt2 deficient murine naive CD4 T cells cultured in Th17-polarizing conditions for 36 hours

Project description:Akt1 and Akt2, isoforms of the serine threonine kinase Akt, are essential for T cell development. However, their role in peripheral T cell differentiation remains undefined. Using mice with germline deletions of either Akt1 or Akt2, we found that both isoforms are important for Th17 differentiation, although Akt2 loss had a greater impact than Akt1. To better understand the consequences of Akt2 deficiency in the setting of in vitro Th17 differentiation, we used microarray analysis to compare the transcriptional landscape of Akt2â/â and WT cells that had been cultured in Th17 polarizing conditions for 36 hours.

2016-07-03 | E-MTAB-4062 | biostudies-arrayexpress

TGF-β specifies TFH versus TH17 cell fates in murine CD4+ T cells through c-Maf (Seq02, bulk-RNAseq)

Project description:Naive murine CD4+ T cells from GREAT/SMART-17A mice were cultured under Th1 or Tfh(1 ng/ml TGF-β)-polarizing conditions in 96-well plates coated with anti-CD3/anti-CD28 for 3.5 days; sorted by flow cytometry on IFNg+ (Th1), or CXCR5-IL17A+ (Th17) and CXCR5+IL17A- (Tfh); and subjected to bulk RNA-seq.

2024-03-01 | GSE198374 | GEO

Transcriptional profiling of IRF4 -/- vs IRF4 +/- T-cells under Th17 polarizing conditions

Project description:Transcriptional profiling of T-cells isolated from spleen of IRF4 -/- mice and cultured under Th17 polarizing conditions for 42 hrs compared to cells similarly isolated and cultured from spleen of IRF4 +/- mice. The aim of the study was to identify global misexpression of genes in IRF4 -/- cells and hence identify key pathways regulated by IRF4 during Th17 differentiation.

2012-09-13 | GSE40726 | GEO

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