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Transcription factors IRF8 and PU.1 are required for follicular B cell development and BCL6-driven germinal center responses

ABSTRACT: Transcription factors IRF8 and PU.1 are required for follicular B cell development and BCL6-driven germinal center responses

PROVIDER: PRJNA526662 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8713560.fastq.gz	Fastqsanger.gz
	SRR8713561.fastq.gz	Fastqsanger.gz
	SRR8713562.fastq.gz	Fastqsanger.gz
	SRR8713563.fastq.gz	Fastqsanger.gz
	SRR8713554.fastq.gz	Fastqsanger.gz

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Similar Datasets

Transcription factors IRF8 and PU.1 are required for follicular B cell development and BCL6-driven germinal center responses

Project description:The IRF and Ets families of transcription factors regulate the expression of a range of genes involved in immune cell development and function. However, the understanding of molecular mechanisms of each family member has been limited due to their redundancy and broad effects on multiple lineages of cells. Here, we report that double deletion of floxed Irf8 and Spi1 (encoding PU.1) by Mb1-Cre (designated DKO mice) in the B cell lineage resulted in severe defects in the development of follicular and germinal center (GC) B cells. Class switch recombination and antibody affinity maturation were also compromised in DKO mice. RNA-seq and ChIP-seq analyses revealed distinct IRF8 and PU.1 target genes in follicular and activated B cells. DKO B cells had diminished expression of target genes vital for maintaining follicular B cell identity and GC development. Moreover, our findings reveal that expression of BCL6, which is critical for development of germinal center B cells, is dependent on IRF8 and PU.1 in vivo, providing a mechanism for the critical role for IRF8 and PU.1 in the development of GC B cells.

2019-03-30 | GSE128166 | GEO

Transcriptional network governed by IRF8 and/or PU.1 in germinal center B cells

Project description:This SuperSeries is composed of the following subset Series: GSE30357: Chip-chip from human diffuse large B cell lymphoma cell lines with IRF8 GSE30358: Mouse B cell lymphoma cell lines:IRF8 knockdown cells vs. Control GSE30519: Chip-chip from mouse diffuse large B cell lymphoma cell lines with IRF8 GSE30520: Chip-chip from mouse diffuse large B cell lymphoma cell lines with PU.1 Refer to individual Series

2011-10-14 | E-GEOD-30359 | biostudies-arrayexpress

Transcription factors IRF8 and PU.1 are required for follicular B cell development and BCL6-driven germinal center responses.

Project description:The IRF and Ets families of transcription factors regulate the expression of a range of genes involved in immune cell development and function. However, the understanding of the molecular mechanisms of each family member has been limited due to their redundancy and broad effects on multiple lineages of cells. Here, we report that double deletion of floxed Irf8 and Spi1 (encoding PU.1) by Mb1-Cre (designated DKO mice) in the B cell lineage resulted in severe defects in the development of follicular and germinal center (GC) B cells. Class-switch recombination and antibody affinity maturation were also compromised in DKO mice. RNA-seq (sequencing) and ChIP-seq analyses revealed distinct IRF8 and PU.1 target genes in follicular and activated B cells. DKO B cells had diminished expression of target genes vital for maintaining follicular B cell identity and GC development. Moreover, our findings reveal that expression of B-cell lymphoma protein 6 (BCL6), which is critical for development of germinal center B cells, is dependent on IRF8 and PU.1 in vivo, providing a mechanism for the critical role for IRF8 and PU.1 in the development of GC B cells.

| S-EPMC6511064 | biostudies-literature

Bcl6 expression specifies the T follicular helper cell program in vivo

Project description:T follicular helper (Tfh) cells play a pivotal role in germinal center reactions, which requires Bcl6 transcription factor. To analyze their relationships with other effector T cell lineages and their stability in vivo, we developed and analyzed a new Bcl6 reporter mouse alone or together with other lineage reporter systems. Assisted with genome-wide transcriptome analysis, we show substantial plasticity of T cell differentiation in the early phase of immune response. At this stage, CXCR5 appears to be expressed in a Bcl6-independent manner. Once Bcl6 is highly expressed, Tfh cells can persist in vivo and some of them develop into memory cells. Together, our results indicate Bcl6 as a bona fide marker for Tfh polarized program. Three group of samples, with 2 biological replicates within each group and total of 6 samples were analyzed.

2012-09-17 | E-GEOD-40068 | biostudies-arrayexpress

Bcl6 expression specifies the T follicular helper cell program in vivo

2012-09-17 | GSE40068 | GEO

ChIP-on-chip of BCL6 in follicular lymphoma

Project description:Identification of BCL6 target genes in primary follicular lymphomas by ChIP-on-chip.

2016-12-31 | GSE29165 | GEO

Transcription profiling of chicken Bcl6 deficient DT40 B cell line to investigate the targets of Bcl6 which is required for germinal center formation

Project description:The transcription factor Bcl6 is required for germinal center formation and deregulated expression of Bcl6 has been observed in lymphomas. To gain insight to the function of Bcl6 in terminal differentiation of B cells to plasma cells and to investigate the targets of Bcl6, we established a Bcl6 deficient DT40 B cell line.

2010-02-17 | E-MEXP-2062 | biostudies-arrayexpress

Lineage-specific functions of Bcl6 Â in immunity and inflammation are mediated through distinct biochemical mechanisms

Project description:The transcription factor Bcl6 orchestrates the germinal center reaction through its actions in B and T cells, and regulates inflammatory signaling in macrophages. We report that genetic replacement by mutant Bcl6, which cannot bind corepressors to its BTB domain, disrupted Â germinal center formation and immunoglobulin affinity maturation, due to a defect in B cell Â proliferation and survival. In contrast, BTB loss of function had no effect on T follicular helper cell differentiation and function, nor other T helper subsets. Bcl6 null mice displayed a lethal inflammatory phenotype, whereas BTB mutant mice experienced normal healthy lives with no inflammation. Bcl6 repression of inflammatory responses in macrophages was accordingly independent of the BTB domain repressor function. Bcl6 thus mediates its actions through lineage-specific biochemical functions. ChIP-seq for Bcl6, SMRT and BCOR in germinal center B cells

2013-03-03 | E-GEOD-43350 | biostudies-arrayexpress

Genome-wide analysis identifies Bcl6 repression of the IL-7R/STAT5 axis during T follicular helper (Tfh) cell differentiation

Project description:T follicular helper (Tfh) cell is a unique T cell subset specialized in promoting germinal center reactions. Bcl6 has been identified as an obligatory transcription factor in Tfh cells; however, the molecular mechanism underlying Bcl6 function still remains unknown. Here, we combined genome-wide Bcl6 occupancy and transcriptome profiling to systemically analyze Bcl6 targets in Tfh cells. We found that Bcl6 exhibits unique binding preferences in Tfh cells from those in Th9, B cells and macrophage and its binding is closely associated with decrease in 5-hydroxymethylcytosine (5hmC). Importantly, Bcl6 directly binds to the IL-7R/CD127 gene and suppresses its expression. Bcl6 also binds the same sequences recognized by signal transducer and activator of transcription (STAT) 5, downstream of IL-7R. Bcl6 promotes CD127loPDhi Tfh cell differentiation; deletion of the Bcl6 gene in T cells results in enhanced IL-7R-STAT5 signaling and substantial expansion of CD127hiPDlo non-Tfh cells. Our study thus systemically examines Bcl6-controlled regulatory networks and provides novel insights into its biological functions in Tfh cells.

2016-01-31 | GSE72188 | GEO

The BCL6 RD2 domain governs commitment of activated B-cells to form germinal centers

Project description:Our data demonstrated that Bcl6 directly binds and represses trafficking receptors S1pr1 and Grp183 by recruiting Hdac2 through the RD2 domain. Deregulation of these genes impairs B-cell migration and may contribute to the Germinal Center failure in Bcl6RD2MUT mice. RNAseq was performed in endogenous BCL6-depleted OCI-LY1 cells rescued with either WT or RD mutant BCL6 (N=3 for each group).

2014-09-14 | E-GEOD-58365 | biostudies-arrayexpress

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