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Transcriptome profiling of Blimp-1-deficient B cells from distinct divisions during plasma cell differentiation

ABSTRACT: Transcriptome profiling of Blimp-1-deficient B cells from distinct divisions during plasma cell differentiation

PROVIDER: PRJNA561798 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10017700_1.fastq.gz	Fastqsanger.gz
	SRR10017700_2.fastq.gz	Fastqsanger.gz
	SRR10017800_1.fastq.gz	Fastqsanger.gz
	SRR10017800_2.fastq.gz	Fastqsanger.gz
	SRR10017701_1.fastq.gz	Fastqsanger.gz

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Transcriptome profiling of Blimp-1-deficient B cells from distinct divisions during plasma cell differentiation

Project description:To examine the cell division that Blimp-1 functioned during B cell differentiation we adoptively transferred CellTrace Violet labeled Blimp-1-deficient or control B cells into congenically disparate uMT hosts. Following transfer, mice were innoculated with LPS to induce B cell differentiation and 72 hours later cells from distinct divisions were FACS sorted for RNA-seq

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miRNA expression in Blimp-1-deficient dendritic cells

Project description:Expression of Blimp-1 was specifically deleted in dendritic cells (DCs) by breeding Blimp-1 flox and CD11c-CRE mice. MiRNA expression was evaluated and compared from DCs, CD4+ T cells and total B cells from spleens of control and Blimp-1 KO mice. Age-matched (6-10 weeks old) female mice from control and Blimp-1 KO mice were sacrificed and spleens were collected. CD11chi/MHCIIhi DCs, CD4+TCRb+ T cells and B220+ B cells were sorted by FACSaria. MiRNA was measured from the total RNA preparation.

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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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Gene expression in LCMV-specific Blimp-1 deficient effector CD8+ T cells compared to wildtype effector CD8+ T cells

Project description:Antigen-specific effector CD8+ T cells deficient in Blimp-1 (Prdm1) do not acquire maximal effector functions, evade terminal differentiation, and more rapidly acquire some hallmark properties of memory CD8+ T cells. In this study, we compared the gene expression profiles of wildtype and Prdm1-/- LCMV-specific effector CD8+ T cells to better understand the molecular mechanisms underlying this striking phenotype. DNA microarray analysis was performed of DbGP33-41 and DbNP396-404 tetramer-positive effector CD8+ T cells FACS-sorted at day 8 post-LCMV infection from four independent samples of either Blimp-1 conditional knockout mice (CKO; Blimp-1flox/flox x GranzymeB-cre+) or wildtype (WT) littermate controls.

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2013-10-10 | E-GEOD-48358 | biostudies-arrayexpress

Epigenetic modifications induced by Blimp-1 regulate CD8+ T cell memory progression during acute virus infection

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