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

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

PROVIDER: PRJNA838387 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19215955_1.fastq.gz	Fastqsanger.gz
	SRR19215955_2.fastq.gz	Fastqsanger.gz
	SRR19215956_1.fastq.gz	Fastqsanger.gz
	SRR19215956_2.fastq.gz	Fastqsanger.gz
	SRR19215957_1.fastq.gz	Fastqsanger.gz

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

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

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

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

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ATAC-seq 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.

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

2023-02-01 | GSE203065 | 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

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

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.

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Expression data from WT and Tbx21-/- in vivo TFH cells versus TH1 cells

Project description:Follicular helper T cells (TFH), known as the primary helpers of the germinal center (GC) reaction, promote the humoral immune response to defend against various pathogens. Under conditions of infection by different types of pathogens, many shared transcription factors (TFs), such as Bcl-6, TCF-1 and Maf, are broadly expressed in TFH cells, orchesting TFH cell differentiation and function. In addtion, TFH cells also coexpress environmentally specific TFs as their conventional T cell counterparts (such as T-bet, GATA-3 or ROR-γt, which are expressed in Th1, Th2 or Th17 cells, respectively). This phenomenon indicates the complexity and environmental adaptivity of the TFH cell response. However, the extent to which the TFH cell response relies on these environmentally specific TFs is not completely understood. Here, we found that transcription factor T-bet was specifically expressed in type I but not type II TFH cells and that the T-bet-IFN-γ axis was essential for the maintenance of TFH cells, promoting their proliferation and inhibiting their apoptosis during acute viral infection. Microarray analysis showed both similarities and differences in transcriptome dependency on T-bet in TFH and Th1 cells, suggesting the distinctive role of T-bet in TFH cells. Collectively, our findings reveal an important and specific supporting role for T-bet in type I TFH cell response, which can help us gain a depper understanding of TFH cell subsets.

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Id2 is required for antiviral Th1 cell differentiation and represses Tfh cell differentiation

Project description:Differentiation of naive CD4+ T cells into T-helper (Th) effector subsets is critical for protection against pathogens. Together, E-protein transcription factors and the inhibitor-of-DNA binding (Id) proteins are important arbiters of T cell development, but their role in the differentiation of Th1 and Tfh cells is not well understood. Th1 cells show robust Id2 expression compared to Tfh cells, and RNAi depletion of Id2 increased Tfh cell frequencies and germinal center responses, while impairing Th1 cell accumulation during viral infection. Further, Th1 cell differentiation was blocked by genetic ablation of Id2, leading to E-protein dependent accumulation of effector cells with 78% of Th1-associated genes showing diminished expression and a concurrent enrichment of the Tfh gene-expression program. The Tfh-defining transcriptional repressor Bcl6 bound to the Id2 locus inhibiting expression, providing a mechanism by which bimodal expression of Id2 in Tfh and Th1 cells can be established. Thus, Id2 is critical in enforcing the reciprocal development of Th1 and Tfh cell fates. We used microarray to assess the changes in gene expression between Id2-sufficient and -deficient Th1 and Tfh cells.

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