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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE83283 | GEO | 2017/06/01

SECONDARY ACCESSION(S): PRJNA325482

REPOSITORIES: GEO

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

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BLIMP-1 is insufficient to induce antibody secretion in the absence of IRF4

Project description:Differentiation of B cells into antibody secreting cells (ASCs), plasmablasts and plasma cells, is regulated by a network of transcription factors. Within this network factors including PAX5 and BCL6 prevent ASC differentiation and maintain the B cell phenotype whereas BLIMP-1 and high IRF4 expression promote plasmacytic differentiation. BLIMP-1 is thought to induce immunoglobulin secretion. While IRF4 is needed for the survival of ASCs, its role in the regulation of antibody secretion has been controversial. BCL6-deficient DT40 B cell line has upregulated BLIMP-1 expression and secrete antibodies. In order to study the role of IRF4 in regulation of antibody secretion we have created a double knockout (DKO) DT40 B cell line deficient in both IRF4 and BCL6. This DKO cell line did not upregulate PRDM1 (the gene encoding for BLIMP-1) expression or secrete IgM. Even enforced BLIMP-1 expression in DKO cells or IRF4-deficient cells could not induce IgM secretion while it did in WT cells. However, enforced IRF4 expression in DKO cells induced strong IgM secretion. Our findings support a model where IRF4 expression in addition to BLIMP-1 expression is required to induce antibody secretion.

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IRF4-dependent division-coupled reprogramming events [IRF4cKO.RNAseq]

Project description:To assess the timing and scope of IRF4–dependent reprogramming in vivo, CTV-labeled IRF4–sufficient and –deficient B cells were transferred into mMT hosts. One day later, hosts were challenged with 50 mg LPS. Three days post-LPS challenge, transferred cells were recovered and sorted from divisions 0, 1, 3, 4, 5, and 6 as determined by CTV dilution for RNA–seq.

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Project description:IRF4 is mainly expressed in immune cells, including B cell, T cell, macrophage and dendritic cell. Previous study showed that IRF4 plays important roles in regulating the differentiation and maturation of immune cells. Recently, our and other`s studies revealed that IRF4 involved in the pathogenesis of cardiac hypertrophy, cerebral ischemic reperfusion injury and metabolic disorder. However, the function of IRF4 in VSMC and neointima formation was largely unknown. We found that IRF4 expression was dramatically decreased in the VSMCs of mouse carotid artery. More importantly, using global IRF4 deficient mouse (KO), we demonstrated that IRF4 deficiency significantly increased VSMC proliferation, migration and neointima formation compared with wild type mice (WT) in response to injury. To evaluate the underlying mechanism by which IRF4 promotes VSMC proliferation and migration after vascular injury, IRF4 KO and WT mice were subjected to wire-injury and the carotid arteries were collected at 14 days post-injury. We combined 3-5 vessels for one sample, and 3 samples for each phenotype. Subsequently, a total of 400ng RNA was used following Affymetrix instruction and 10 ug of cRNA were hybridized for 16 hr at 45°. GeneChips were scanned using the Scanner 7G and the data was analyzed with Expression Console using Affymetrix default analysis settings and global scaling as normalization method. RMA analysis was employed to evaluate the gene expression. We used microarrays to detect the global gene expression in the carotid arteries of IRF4 knockout mice (IRF4 KO) compared with wild type mice (WT) at 14 days post-injury and identified distinct classes of altered genes

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

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