P38α activation is essential for germinal center B cell to plasma cell differentiation
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA705180 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13794607_1.fastq.gz | Fastqsanger.gz | |||
| SRR13794607_2.fastq.gz | Fastqsanger.gz | |||
| SRR13794608_1.fastq.gz | Fastqsanger.gz | |||
| SRR13794608_2.fastq.gz | Fastqsanger.gz | |||
| SRR13794609_1.fastq.gz | Fastqsanger.gz |
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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).
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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.
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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.
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