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Transcriptomic profiling of transduced human CD4 T cell expressing different IRF4 mutants

ABSTRACT: Transcriptomic profiling of transduced human CD4 T cell expressing different IRF4 mutants

PROVIDER: PRJNA887470 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21820041_1.fastq.gz	Fastqsanger.gz
	SRR21820041_2.fastq.gz	Fastqsanger.gz
	SRR21820042_1.fastq.gz	Fastqsanger.gz
	SRR21820042_2.fastq.gz	Fastqsanger.gz
	SRR21820043_1.fastq.gz	Fastqsanger.gz

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Transcriptomic profiling of transduced human CD4 T cell expressing different IRF4 mutants

Project description:A heterozygous IRF4 missense variant located within the interferon activation domain of the encoded IRF4 protein (mutIAD) was identified in three patients from a multigenerational family suffering from a novel autosomal dominant disease predominantly presenting as a hypogammaglobulinemia with recurrent infections. In these experiments we aimed to investigate the effect of this IRF4 mutation on the transcriptome of T lymphocytes.

2023-03-06 | GSE214888 | GEO

Gene profiling data of CD4+ T cells transduced with FOXP3 and candidate cofactors

Project description:The transcription factor FoxP3 partakes dominantly in the specification and function of FoxP3+ CD4+ T regulatory cells (Tregs), but is neither strictly necessary nor sufficient to determine the characteristic Treg transcriptional signature. Computational network inference and experimental testing assessed the contribution of several other transcription factors (TFs). Enforced expression of Helios or Xbp1 elicited specific signatures, but Eos, Irf4, Satb1, Lef1 and Gata1 elicited exactly the same outcome, synergizing with FoxP3 to activate most of the Treg signature, including key TFs, and enhancing FoxP3 occupancy at its genomic targets. Conversely, the Treg signature was robust to inactivation of any single cofactor. A redundant genetic switch thus locks-in the Treg phenotype, a model which accounts for several aspects of Treg physiology, differentiation and stability. To study the impact of FoxP3 and its candidate cofactors (Eos, Gata1, Helios, Irf4, Lef1, Satb1, Xbp1) on the expression of the Treg transcriptional signature, CD4+ conventional T cells (Tconv) activated with anti-CD3+CD28 beads were retrovirally transduced with cDNAs encoding FOXP3, candidate TFs, or a combination of FOXP3 and candidate TFs. After 3 days in culture, the transduced cells were sorted into Trizol, and RNA was purified, labeled and hybridized to Affymetrix arrays.

2012-08-23 | E-GEOD-40274 | biostudies-arrayexpress

In vivo microarray expression data from WT, Irf4-/- and checkpoint blockade treated Irf4-/- TEa CD4+ T cells

Project description:Previously we found that Irf4-deficient T cells were dysfunctional and unable to reject heart allografts and checkpoint blockade treatment could reinvigorate dysfunctional Irf4-deficient T cells and enable them reject heart allografts. But shortly after the reinvigoration those T cells went back to dysfunctional state. TCR-transgenic TEa CD4+ T cells (B6 background) recognize a Balb/c I-Eα allopeptide presented by B6 antigen presenting cells, and were used to assess the effects of immune checkpoint blockades on Irf4-deficient alloreactive T cells. WT, Irf4-/- and checkpoint blockade treated Irf4-/- TEa CD4+ T cells were isolated from Balb/c heart transplanted B6 mice, followed by microarray analysis. To define un-restored gene expressions in Irf4-deficient alloreactive T cells upon immune checkpoint blockades, we compared genes expression level among three groups. We revealed that checkpoint blockade restored the expression levels of the majority of wild-type T cell-expressed genes in Irf4-/- T cells, indicating the reinvigoration of Irf4-/- T cells. The remaining un-restored genes following checkpoint blockade, though minimal in number, may be responsible for the reinvigorated Irf4-/- T cells to become re-dysfunction.

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Microarray expression data from WT and Irf4-/- CD4+ T cells after activation

Project description:To define molecular basis underlying dysfunction of Irf4-deficient T cells. We found that Irf4-deficient T cells were dysfunctional and unable to infiltrate and reject heart allografts, and then investigated the molecular basis underlying dysfunction of Irf4-deficient T cells. Irf4-deficient and wild type B6 CD4+ T cells were activated in vitro for two days, followed by microarray analysis. We found that dysfunction of Irf4-deficient T cells is not only due to impaired effector differentiation, but also involves an altered transcriptional programme that allows the expression of essential negative regulators of T-cell function.

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

Project description:Interferon regulatory factor 4 (IRF4) is an IRF family transcription factor with critical roles in lymphoid development and in regulating the immune response. IRF4 binds DNA weakly owing to a carboxy-terminal auto-inhibitory domain, but cooperative binding with factors such as PU.1 or SPIB in B cells increases binding affinity, allowing IRF4 to regulate genes containing ETS–IRF composite elements (EICEs; 5'-GGAAnnGAAA-3'). Here we show that in mouse CD4+ T cells, where PU.1/SPIB expression is low, and in B cells, where PU.1 is well expressed, IRF4 unexpectedly can cooperate with activator protein-1 (AP1) complexes to bind to AP1–IRF4 composite (5'-TGAnTCA/GAAA-3') motifs that we denote as AP1–IRF composite elements (AICEs). Moreover, BATF–JUN family protein complexes cooperate with IRF4 in binding to AICEs in pre-activated CD4+ T cells stimulated with IL-21 and in TH17 differentiated cells. Importantly, BATF binding was diminished in Irf4-/- T cells and IRF4 binding was diminished in Batf-/- T cells, consistent with functional cooperation between these factors. Moreover, we show that AP1 and IRF complexes cooperatively promote transcription of the Il10 gene, which is expressed in TH17 cells and potently regulated by IL-21. These findings reveal that IRF4 can signal via complexes containing ETS or AP1 motifs depending on the cellular context, thus indicating new approaches for modulating IRF4-dependent transcription. Genome-wide transcription factors mapping and binding of IRF4, BATF, IRF8, STAT3, JUN etc in WT, Irf4-/- and Batf-/- mice in different cell types (B cells, CD4+ T cells and TH17 cells) cultured with or without IL-21 was conducted. RNA-Seq is conducted in mouse B cells, CD4+ T cells, TH1/TH2/TH9/TH17/Treg.

2012-09-18 | E-GEOD-39756 | biostudies-arrayexpress

Gene profiling data of CD4+ T cells doubly transduced with EOS+LEF1 or GATA1+SATB1

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BATF3-dependent IRF4 binding inhibits FOXP3 in differentiating Tregs

Project description:BATF3 has been shown to inhibit FOXP3 expression in differentiating CD4 T cells, however, the role of IRF4 in this inhibition is unexplored. IRF4 binds DNA weakly on its own and requires interactions with other transcription factors. We investigated how BATF3/IRF4 interactions are necessary for IRF4 binding and BATF3-mediated FOXP3 inhibition.

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Epigenetic profiles of HSCs transduced with control or Runx3-expressing lentivirus

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Expression data of Pioglitazone-, Rosiglitazone-, GW1929- and vehicle-treated CD4+FoxP3- T cells transduced with Foxp3+Pparg1

Project description:Pioglitazone treatment of CD4+FoxP3- T cells transduced with Pparg and Foxp3 up-regulated a set of genes whose products have been implicated in lipid metabolism pathways. To verify the specificity of this treatment, we performed microarray analysis on Foxp3+Pparg1-transduced CD4+FoxP3- T cells after treatment with other PPARg agonists such as Rosiglitazone (TZD) and GW1929 (non-TZD).

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