Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA-sequencing of pre-GC B cells helped by CD4-CrexBcl6fl/+ or CD4-Cre OT-II T cells

ABSTRACT: We analyzed transcriptome differences of antigen-specific pre-GC B cells. We transferred wildtype (CD4-Cre) or BCL6-insufficient (CD4-CrexBcl6fl/+) OT-II T cells into SAP-deficient mice and immunized these mice with NP-OVA. By day 3 post immunization, we sort-purified NP-binding B cells that were developing into GCs and conducted RNA-seq analyses of their transcriptome. NP+IgDlowB220+ pre-GC B cells from recipients of the same group were pooled to sort-purify 4 200-cell repeats. Using a gene expression signature induced by CD40 signaling in B cells for enrichment analysis, we found such CD40-induced gene set expression was significantly deprived in those NP-binding B cells helped by CD4-Cre´Bcl6fl/+ T cells. These data suggest BCL6 insufficiency in T cells leads to impaired CD40L signaling to B cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE180833 | GEO | 2021/07/30

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

RNA-sequencing of BCL6-sufficient and -insufficient OT-II TFH cells

Project description:We analyzed the transcriptome differences of BCL6-sufficient (CD4-Cre) and -insufficient (CD4-CrexBcl6fl/+) OT-II TFH cells. CD4-CrexBcl6fl/+ or control CD4-Cre OT-II T cells were transferred into CD45.1 Sap-/- mice. At day 3 post NP-OVA immunization, CXCR5hiPD-1hi TFH cells were sort-purified from the draining lymph node and prepared for RNA-seq analysis. Two technical repeats of ~200 cells per sample from each of 3 mice were included. BCL6-insufficient TFH cells differentially expressed many genes; among those downregulated were Stim1 and Plcg1, which code for STIM1 and PLCg1, respectively, that both impinge on calcium signaling downstream of TCR activation. Moreover, KEGG pathway analyses revealed that the calcium signaling-related pathway was generally upregulated in wildtype as compared to BCL6-insufficient TFH cells. These data support the notion that BCL6 control follicular T-B interactions by regulating multiple target genes involved in antigen-triggered calcium signaling in T cells.

2021-07-30 | GSE180924 | GEO

RNA-sequencing of pre-GC B cells helped by CD4-CrexBcl6fl/+ or CD4-Cre OT-II T cells

Project description:RNA-sequencing of pre-GC B cells helped by CD4-CrexBcl6fl/+ or CD4-Cre OT-II T cells

| PRJNA749751 | ENA

Gene expression changes in CD4+ thymocytes upon removal of Cullin3

Project description:We report gene expression changes in Cul3 deficient thymic CD4+ T cells We used microarrays to detail the global programme of gene expression changes upon removal of Cul3 during thymic development CD25-, CD1dPBS57-, gdTCR - CD4+ Single positive cells from thymocytes of CD4Cre-Cul3fl/fl (LM) and CD4 Cre+Cul3fl/fl (KO) were sort purified and total RNA was extracted using Trizol and analysed by microarray.

2014-04-05 | E-GEOD-56514 | biostudies-arrayexpress

Expression data from BCL6-YFP-positive Tfh cells, BCL6-YFP-negative Tfh cells, non-Tfh cells, and naïve helper T cells.

Project description:We found that a number of Tfh cells downmodulated BCL6 protein after their development, and we sought to compare the gene expression between BCL6-hi Tfh cells and BCL6-low Tfh cells. CD4+ T cells were sorted from immunized and non-immunized mice for RNA extraction and hybridization on Affymetrix microarrays. Bcl6yfp/+ OT-II cells were transferred to congenic recipient mice, and immunized with NP-OVA in CFA subcutaneously. Seven or ten days after immunization, cells were collected from draining lymph nodes, and sorted on FACSAria by the expression of CXCR5, PD-1 and BCL6-YFP. Naive CD4+ T cells were CD4+ CD44lo CD62Lhi cells from unimmunized mice.

2011-06-02 | E-GEOD-24574 | biostudies-arrayexpress

OT-I T cell activation in Lrrc8af/f and Lrrc8af/f Cd4-Cre;OT-I mice

Project description:Splenocytes were separated from Lrrc8af/f and Lrrc8af/f Cd4-Cre;OT-I mice. The splenocytes were stimulated with indicated peptides (unstime/ SIINFEKL-10pM(NL)/ SIINFEKL-1000pM(NH)/ SIIGFEKL-1000nM(G4)) for 6 hours. The OT-I CD8+ T cells were labeled with Va2-PE/CD8-A700 and sorted for the sequencing.

2023-09-26 | GSE243985 | GEO

Global gene expression profile of CD4+ T cells activated and infected with Tox2- or GFP-only virus under different conditions (RNA-Seq)

Project description:T Follicular helper (Tfh) cell is an effector CD4+ T cell subset specialized in helping B cells in germinal centers (GC) reactions. Although Bcl6 was identified as a Tfh-specific transcription factor essential for their development, the molecular mechanisms underlying Bcl6 regulation and Tfh cell commitment remain unclear. Here, we report that Tox2 transcription factor is highly expressed in Tfh cells, regulated by Bcl6 and STAT3. Forced expression of Tox2 drives Bcl6 expression and Tfh development. Mechanistically, Tox2 directly binds to Tfh-associated genes, including Bcl6, and functions to promote their chromatin accessibility and modulate the activities of other Tfh-regulating factors. Conversely, genetic deletion of Tox2 results in defective Tfh differentiation, and inhibiting both Tox and Tox2 in T cells abolishes Tfh differentiation and GC response. Thus, our results demonstrate that Tox2 is a key transcription factor that regulates Bcl6 expression and Tfh development and suggest a Tox2-Bcl6 axis in feed-forward regulation of Tfh program.

2019-10-30 | GSE136537 | GEO

B cell intrinsic TBK1 is essential for germinal center formation during infection and vaccination

Project description:Germinal center (GC) is a site where somatic hypermutation and clonal selection are coupled for antibody affinity maturation against infections. However, how GCs are formed and regulated is incompletely understood. Here, we identified an unexpected role of Tank-binding kinase-1 (TBK1) as a crucial B-cell-intrinsic factor for GC formation. Using immunization and malaria infection models, we show that TBK1-deficient B cells failed to form GC despite normal Tfh differentiation, although some malaria-infected B-cell-specific TBK1-deficient mice could survive by GC-independent mechanisms. Mechanistically, TBK1 phosphorylation elevates in B cells during GC differentiation and regulates the balance of IRF4/BCL6 expression by limiting CD40 and BCR activation through non-canonical NF-κB and AKTT308 signaling. In the absence of TBK1, CD40 and BCR signaling synergistically enhanced IRF4 expression in Pre-GC leading to BCL6 suppression, therefore failed to form GC. As a result, memory B cells generated from TBK1-deficient B cells fail to confer sterile immunity upon re-infection, suggesting that TBK1 determines B cell fate to promote long-lasting humoral immunity.

2021-12-12 | GSE188659 | GEO

Bcl6 controlled gene expression in naïve CD4 T cells (Tf0)

Project description:Gene expression data from wild-type and Bcl6-/- naive CD4 T cells In order to find genes regulated by Bcl6 in follicular helper T cells Naïve CD4 T cells were sorted from wild-type (WT) and T cell-specific conditional Bcl6-/- (KO) mice-- 8 samples, 4 WT and 4 KO

2015-04-08 | E-GEOD-67622 | biostudies-arrayexpress

Bcl6 controlled gene expression in naïve CD4 T cells (Tfh)

2015-04-08 | E-GEOD-67623 | biostudies-arrayexpress

Gene expression profiling in mature OT-II TCR transgenic CD4 SP thymocytes, either Jmjd3- and Utx-deficient or -sufficient.

Project description:The biological functions of histone demethylases Jmjd3 and Utx remain poorly understood. We assessed such functions in developing T cells, using conditional (CD4-Cre-mediated) gene disruption, by inactivating Kdm6a and Kdm6b, respectively encoding Utx and Jmjd3, in immature CD4+CD8+ thymocytes. We compared microarray gene expression in mature (Va2hi CD24lo) mutant and wild-type CD4+CD8- thymocytes carrying the OT-II TCR transgene. We show that Jmjd3 and Utx redundantly promote H3K27Me3 removal at, and expression of, a specific subset of genes involved in terminal thymocyte differentiation, especially S1pr1, encoding a sphingosine-phosphate receptor required for thymocyte egress. Mature (Va2hi CD24lo) CD4 thymocytes were sorted from freshly prepared single-cell suspensions OT-II TCR transgenic thymocytes deficient for Utx and Jmjd3 (dKO, CD4-Cre conditional deletion of floxed Kdm6a and Kdm6b alleles), and from Cre-negative controls (wild-type). Total RNA was extracted from sorted thymocytes using the RNeasy Plus Mini Kit (Qiagen) and processed for microarray analyses (Affymetrix Mouse Exon 1.0 ST array) at the NCI microarray facility, following the manufacturer’s recommendation. Data is generated from 3 replicates from each experiment.

2015-09-17 | E-GEOD-70363 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data