Tbet regulates the accessible chromatin of Be1 B cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA487609 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7748180_1.fastq.gz | Fastqsanger.gz | |||
| SRR7748180_2.fastq.gz | Fastqsanger.gz | |||
| SRR7748190_1.fastq.gz | Fastqsanger.gz | |||
| SRR7748190_2.fastq.gz | Fastqsanger.gz | |||
| SRR7748181_1.fastq.gz | Fastqsanger.gz |
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Project description:To investigate the role of Tbet in B cell differentiation to "effector-like" antibody secreting cells (ASC's) we utilized an ex vivo culture system to differentiate B cells in the presence of Th1 (Be1) or Th2 (Be2) polarized T cells. To determine the role of Tbet in Be1 cell differentiation we performed ATAC-seq on Wt Be1 and Tbet negative (TbetNeg) Be1 cells and Wt Be2 and Tbet negative (TbetNeg) Be2 cells. Collectively, these data show that T-bet serves as master regulator for the Be1 cell fate and is required to program chromatin accessibility during ASC differentiation in Be1 cells.
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Project description:To investigate the role of Tbet in B cell differentiation to "effector-like" antibody secreting cells (ASC's) we utilized an ex vivo culture system to differentiate B cells (Be1 cells) in the presence of Th1 polarized T cells. To determine the role of Tbet in Be1 cell differentiation we performed RNA-seq on Wt Be1 and Tbet negative (TbetNeg) Be1 cells. Collectively, these data show that T-bet serves as master regulator for the Be1 cell fate and is required for induction of genes required for ASC differentiation in Be1 cells.
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Project description:We examined the accessible chromatin differences between circulating B cell subsets post-vaccination. Using FCRL5 as a marker of Tbet expressing B cells, we sorted FCRL5+ (Tbet+) and FCRL5- (Tbet-) memory B cells, and antibody secreting plasmablasts at day 7 and day 14 post-vaccination. Additionally, we used H1 B cell tetramers to track cells responding to the influenza vaccine in a subset of samples. These data provide insights into the accessible chromatin landscape of distinct B cell subsets that respond to influenza vaccination.
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Project description:B cells cultured in the presence of Th1 CD4 T cells (Be1) or Th2 CD4 T cells (Be2) lead to distinct phenotypic outcomes. To determine when the phenotypic differences emerged, IgD positive and IgD negative Be1 and Be2 cells were isolated from cultures derived from 3 independent donors and RNA-seq performed. These data define the transcriptional differences of Be1 and Be2 cells ad distinct differentiation stages and show that Be1 B cells contain a pre-ASC signature that is absent from Be2 B cells.
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Project description:The role of antibody and B cells in preventing infection is established. In contrast, the role of B cell responses in containing chronic infections remains poorly understood. IgG2a (IgG1 in humans) can prevent acute infections and T-bet promotes IgG2a isotype switching. However, whether IgG2a and B cell-expressed T-bet influence the host-pathogen balance during persisting infections is unclear. Here we demonstrate that B cell specific loss of T-bet prevents control of persisting viral infection. T-bet in B cells not only controlled IgG2a production, but also mucosal localization, proliferation, glycosylation, and a broad transcriptional program. T-bet controlled a broad antiviral program in addition to IgG2a since T-bet in B cells was imÂportant even in the presence of virus-specific IgG2a. Our data supports a model in which T-bet is a universal controller of antiviral immunity across multiple immune lineages. Naïve, Tbet+, and Tbet- Memory B cells were assayed for gene expression Tbet GFP reporter mice were infected with LCMV clone 13, and target B cell populations were sorted from splenocytes at day 10 post-infection
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2016-06-15 | E-GEOD-66390 | biostudies-arrayexpress
Project description:we combined Assay for Transposase-Accessible Chromatin and lattice light-sheet PALM microscopy (3D ATAC-PALM) to selectively image key features of the 3D accessible genome in single cells. We found that accessible chromatin domains (ACDs) form spatially segregated clusters in the nucleus. Rapid depletion of CTCF or Cohesin (RAD21 subunit) induced extensive 3D spatial mixing of ACD clusters and reduced physical separation between ACDs within chromosomes. Experimental perturbations and modeling suggest that both weak, multivalent, dynamic protein-protein interactions together with loop extrusion influence ACD organization. Live-cell studies suggest that ACD clustering regulates transcription factor binding site distribution, target search kinetics and binding dynamics. Here we report the ATAC-seq results from Tn5 PA549 and nextera Tn5 upon various chemical and genetic perturbations.
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