Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA311335 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR3158110.fastq.gz | Fastqsanger.gz | |||
| SRR3158120.fastq.gz | Fastqsanger.gz | |||
| SRR3158130.fastq.gz | Fastqsanger.gz | |||
| SRR3158140.fastq.gz | Fastqsanger.gz | |||
| SRR3158150.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 61 |
Similar Datasets
Project description:E2A is an essential regulator of early B-cell development. Here we demonstrated that E2A together with E2-2 controlled germinal-center B-cell and plasma cell development. As shown by identification of regulated E2A,E2-2 targets in activated B-cells, these E-proteins directly activated genes with important functions in germinal-center B-cells and plasma cells by inducing or maintaining DNase I hypersensitive sites. Through controlling multiple enhancers in the Igh 3’ regulatory region and Aicda locus, E-proteins regulated class switching by inducing both Igh germline transcription and AID expression. By regulating 3’ Igk enhancers and a distal element at the Prdm1 (Blimp1) locus, E-proteins contributed to Igk, Igh and Prdm1 activation in plasmablasts. These data identified E2A and E2-2 as central regulators of B-cell immunity.
2016-06-01 | GSE77744 | GEO
Project description:E2A is an essential regulator of early B-cell development. Here we demonstrated that E2A together with E2-2 controlled germinal-center B-cell and plasma cell development. As shown by identification of regulated E2A,E2-2 targets in activated B-cells, these E-proteins directly activated genes with important functions in germinal-center B-cells and plasma cells by inducing or maintaining DNase I hypersensitive sites. Through controlling multiple enhancers in the Igh 3â regulatory region and Aicda locus, E-proteins regulated class switching by inducing both Igh germline transcription and AID expression. By regulating 3â Igk enhancers and a distal element at the Prdm1 (Blimp1) locus, E-proteins contributed to Igk, Igh and Prdm1 activation in plasmablasts. These data identified E2A and E2-2 as central regulators of B-cell immunity. 56 samples in total: A) 38 RNA-Seq samples in 5 cell types: Follicular B cells (FO B cell, 2 genotypes, 2 replicates each) Activated B cells (Act B cell, 2 genoytpes, 6 stimulations, 2 replicates each) Pre-Plasmablasts (Pre-PB, 1 genotype, 2 stimulations, 2 replicates each) Plasmablasts (PB, 1 genotype, 2 stimulations, 2 replicates each) Germline Center B cells (GC B cell, 1 genotype, 2 replicates); B) 13 ChIP-Seq samples in 5 cell types: FO B cell (E2A, 2 crosslinking types, 1 replicate each) Act B cell (E2A, 2 crosslinking types, 2 stimulations, 1 replicate each; H3K27ac, 1 crosslinking type, 1 stimulation, 2 genotypes, 1 replicate each) Pre-PB (E2A, 2 crosslinking types, 1 stimulation, 1 replicate each) PB (E2A, 2 crosslinking types, 1 stimulation, 1 replicate each) Mature B cell (input); C) 5 ATAC Seq samples in 2 cell types: Act B cell (2 stimulations, 2 genotypes, 1 replicate each), Pre-PB (1 stimulation, 1 genotype, 1 replicate).
2016-06-01 | E-GEOD-77744 | biostudies-arrayexpress
Project description:Humoral immunity requires the generation of high-affinity antibodies, which involves the generation of germinal centres (GC) promoting class switch and affinity maturation of antigen-specific B cells, and the differentiation of long-lived plasma cells. This multi-layered process is tightly controlled by the activity of a transcriptional network including Bcl6, essential for the development of GC, and Blimp1, required for the differentiation of plasma cells. Here, we reveal an additional layer of complexity by demonstrating that dynamic changes in E-protein activity mediated by Id3 govern both GC and plasma cell differentiation. We show that down-regulation of Id3 expression in B cells in essential for releasing E2A and E2-2, the combined activity of which is required for both GC B cell and plasma cell differentiation. We demonstrate that this pathway controls the expression of multiple key factors required for antigen-induced B cell differentiation, including Blimp1, Xbp1, Mef2b and CXCR4 and is therefore critical for establishing the transcriptional network that controls GC B cell and plasma cell differentiation. Genome binding of transcription factor E2A
2016-05-13 | E-GEOD-72828 | biostudies-arrayexpress
Project description:Humoral immunity requires the generation of high-affinity antibodies, which involves the generation of germinal centres (GC) promoting class switch and affinity maturation of antigen-specific B cells, and the differentiation of long-lived plasma cells. This multi-layered process is tightly controlled by the activity of a transcriptional network including Bcl6, essential for the development of GC, and Blimp1, required for the differentiation of plasma cells. Here, we reveal an additional layer of complexity by demonstrating that dynamic changes in E-protein activity mediated by Id3 govern both GC and plasma cell differentiation. We show that down-regulation of Id3 expression in B cells in essential for releasing E2A and E2-2, the combined activity of which is required for both GC B cell and plasma cell differentiation. We demonstrate that this pathway controls the expression of multiple key factors required for antigen-induced B cell differentiation, including Blimp1, Xbp1, Mef2b and CXCR4 and is therefore critical for establishing the transcriptional network that controls GC B cell and plasma cell differentiation. Transcriptional profiling of wild type, Id3 knockout and E2A/E22 double knockout B cells using RNA sequencing
2016-05-13 | E-GEOD-72831 | biostudies-arrayexpress
Project description:Humoral immunity requires the generation of high-affinity antibodies, which involves the generation of germinal centres (GC) promoting class switch and affinity maturation of antigen-specific B cells, and the differentiation of long-lived plasma cells. This multi-layered process is tightly controlled by the activity of a transcriptional network including Bcl6, essential for the development of GC, and Blimp1, required for the differentiation of plasma cells. Here, we reveal an additional layer of complexity by demonstrating that dynamic changes in E-protein activity mediated by Id3 govern both GC and plasma cell differentiation. We show that down-regulation of Id3 expression in B cells in essential for releasing E2A and E2-2, the combined activity of which is required for both GC B cell and plasma cell differentiation. We demonstrate that this pathway controls the expression of multiple key factors required for antigen-induced B cell differentiation, including Blimp1, Xbp1, Mef2b and CXCR4 and is therefore critical for establishing the transcriptional network that controls GC B cell and plasma cell differentiation.
2016-05-13 | GSE72831 | GEO
Project description:Humoral immunity requires the generation of high-affinity antibodies, which involves the generation of germinal centres (GC) promoting class switch and affinity maturation of antigen-specific B cells, and the differentiation of long-lived plasma cells. This multi-layered process is tightly controlled by the activity of a transcriptional network including Bcl6, essential for the development of GC, and Blimp1, required for the differentiation of plasma cells. Here, we reveal an additional layer of complexity by demonstrating that dynamic changes in E-protein activity mediated by Id3 govern both GC and plasma cell differentiation. We show that down-regulation of Id3 expression in B cells in essential for releasing E2A and E2-2, the combined activity of which is required for both GC B cell and plasma cell differentiation. We demonstrate that this pathway controls the expression of multiple key factors required for antigen-induced B cell differentiation, including Blimp1, Xbp1, Mef2b and CXCR4 and is therefore critical for establishing the transcriptional network that controls GC B cell and plasma cell differentiation.
2016-05-13 | GSE72828 | GEO
Project description:B cells provide humoral immunity by differentiating into antibody-secreting plasma cells, a process that requires cellular division and is linked to DNA hypomethylation. Conversely, little is known about how de novo deposition of DNA methylation affects B cell fate and function. Here we show that genetic deletion of the de novo DNA methyltransferases Dnmt3a and Dnmt3b (Dnmt3-deficient) in mouse B cells results in normal B cell development and maturation, but increased cell activation and expansion of the germinal center B cell and plasma cell populations upon immunization. Gene expression is mostly unaltered in naive and germinal center B cells, but dysregulated in Dnmt3-deficient plasma cells. Differences in gene expression are proximal to Dnmt3-dependent DNA methylation and chromatin changes, both of which coincide with E2A and PU.1-IRF composite-binding motifs. Thus, de novo DNA methylation limits B cell activation, represses the plasma cell chromatin state, and regulates plasma cell differentiation.
2017-12-31 | GSE89471 | GEO
Project description:Protective immune responses to many pathogens depend on the development of high affinity antibody-producing plasma cells in germinal centers. Transgenic models suggest that there is a stringent affinity-based barrier to plasma cell development. Whether a similar high affinity barrier regulates plasma cell development under physiologic circumstances, and the nature of the plasma cell fate decision has not been defined precisely. Here we use a fate mapping approach to examine the relationship between germinal center (GC) B cells selected to undergo additional rounds of affinity maturation, germinal center pre-plasma cells and plasma cells. The data show that initial plasma cell selection overlaps with germinal center B cell selection, but that the plasma cell compartment accumulates a less diverse and higher affinity collection of antibodies over time. Thus, whereas the GC continues to diversify over time, affinity-based pre-plasma cell selection sieves the germinal center to enable accumulation of a more restricted group of high affinity antibody secreting plasma cells.
2023-11-02 | GSE246382 | GEO
Project description:p38α activation is essential for germinal center B cell to plasma cell differentiation
| PRJNA705180 | ENA
Project description:IgE plays an essential role in the pathogenesis of allergies and its production is strongly regulated. A transient IgE germinal center phase and lack of IgE memory cells limit the generation of pathogenic IgE, but this can be overcome by sequential switching of IgG1 cells to IgE. We investigated which population of IgG1 cells can give rise to IgE-producing cells in memory responses. We identified three populations of IgG1 memory B cells (DP:CD73+CD80+, SP:CD73-CD80+, DN:CD73-CD80-) that generate IgE plasma cells of high or low affinity, but none gives rise to IgE germinal center cells or IgE memory cells. The two memory IgG1 populations differ however in their ability to differentiate into IgG1 plasma cells and germinal center cells, and to expand the IgG1 memory B cell pool. To explore the molecular mechanisms that may explain the distinct functions of IgG1 memory B cell subsets we compared their expression by transcriptome analysis using next generation sequencing.
2017-07-03 | GSE83436 | GEO