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Transcriptional profiling of Follicular B cells (FoB) in control and T follicular regulatory cell deficient mice

ABSTRACT: Transcriptional profiling of Follicular B cells (FoB) in control and T follicular regulatory cell deficient mice

PROVIDER: PRJNA967662 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24445649_1.fastq.gz	Fastqsanger.gz
	SRR24445649_2.fastq.gz	Fastqsanger.gz
	SRR24445650_1.fastq.gz	Fastqsanger.gz
	SRR24445650_2.fastq.gz	Fastqsanger.gz
	SRR24445651_1.fastq.gz	Fastqsanger.gz

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Transcriptional profiling of Follicular B cells (FoB) in control and T follicular regulatory cell deficient mice

Project description:We isolated Follicular B cells from naïve and Brucella infected mice to determine how T follicular regulatory cells alter the B cell response to infection.

2023-08-31 | GSE231772 | GEO

Glutathione-dependent redox balance characterizes the distinct metabolic properties of follicular and marginal zone B cells

Project description:The metabolic principles underlying the differences between follicular and marginal zone B cells (FoB and MZB, respectively) are not well understood. Here we show, by studying mice with B cell-specific ablation of the catalytic subunit of glutamate cysteine ligase (Gclc), that glutathione synthesis affects homeostasis and differentiation of MZB to a larger extent than FoB, while glutathione-dependent redox control contributes to the metabolic dependencies of FoB. Specifically, Gclc ablation in FoB induces metabolic features of wild-type MZB such as increased ATP levels, glucose metabolism, mTOR activation and protein synthesis. Furthermore, Gclc-deficient FoB have a block in the mitochondrial electron transport chain (ETC) due to diminished complex I and II activity and thereby accumulate the tricarboxylic acid cycle metabolite succinate. Finally, Gclc deficiency hampers FoB activation and antibody responses in vitro and in vivo, and induces susceptibility to viral infections. In summary, Gclc is required to ensure the development of MZB, the integrity of the mitochondrial ETC in FoB and it is crucial for antibody-mediated immunity.

2022-01-25 | GSE194419 | GEO

Transcriptome profiling of H3K27me3 demethylase deficient B cells

Project description:To assess how H3K27me3 demethylases, UTX and JMJD3, regulate B cell and plasma cell trasncriptomes. RNA-seq was performed on the following populations from control (CreCtrl) and double knockout (dKO) mice: 1) naïve marginal zone B (MZB) cells and follicular B (FOB) cells from control (CreCtrl) and double knockout (dKO) mice, 2) PC generated after three days of ex vivo culture of MZB or FOB cells, 3) PC generated at three days post in vivo stimulation with LPS

2022-02-01 | GSE185095 | GEO

Differential gene expression profiling of conventional (Tconv), regulatory (Treg), follicular (TFH) helper and follicular regulatory (TFR) T-cells from control vs OX40L-Jagged-1 treated NZBWF1/j mice

Project description:Differential gene expression profiling of conventional (Tconv), regulatory (Treg), follicular (TFH) helper and follicular regulatory (TFR) T-cells from control vs OX40L-Jagged-1 treated NZBWF1/j mice

2022-03-17 | GSE181433 | GEO

Transcriptional profiling of wildtype versus Themis2-deficient follicular B cells

Project description:Transcriptional profiling of wildtype versus Themis2-deficient follicular B cells

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Gene expression profile of FoxP3+ CD4+ follicular regulatory T cells

Project description:Follicular regulatory T cells (TFR) are a major cellular source of negative regulation of GC antibody responses. Blimp1 is expressed by the majority of TFR cells within B cell follicles during immune responses, as well as by other tissue-specific subsets of effector Treg (eTreg). However, the potential impact of FoxP3-specific Blimp1 deletion on TFR differentiation and suppressive activity has not been evaluated. To better understand the role of Blimp1 in regulation of TFR differentiation and function, we profiled the differential gene expression in Blimp1-deficient TFR cells compared to WT control TFR cells.

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Transcriptional profiling of wildtype versus Themis2-deficient follicular B cells

Project description:This RNA-seqexperiment was designed to find transciptional differences between wildtype and Themis2-deficient B cells either directly ex-vivo or stimulated for 6 h with various stimuli in vitro. It is part of a larger study on the function of Themis2 in B cells. Therefore splenic, live, B220+ CD93- IgM+ CD23+ follicular B cells were sorted by flow cytometry from wildtype or Themis2-deficient (Themis2KO/KO) C57BL/6J mice. Unstimulated samples were were lysed directly after the sort. Stimulated samples were stimulated in vitro for 6 h at 37 degree Celsius at a concentration of 3 million cells/mL with either 10 microgram/mL anti-IgM or 10 microgram/mL LPS or 1 microgram/mL CD40L with 0.1 microgram/mL IL-4 and then lysed. RNA was extracted using Trizol reagent (Life Technologies) and cleaned up using the RNEasy Mini Kit (Quiagen). Single end, unstranded, poly-A-enriched libraries were made using the TruSeq RNA sample preparation kit (Illumina). Samples were analysed with an Illumina HiSeq 2000, collecting 13.2 to 76.1 million reads of 75 bases per sample.

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Follicular B (FoB) cells purified from miR-17-92 transgenic mice

Project description:We have generated a miR-17-92 transgenic allele (termed miR-17-92 Tg) whose expression can be turned on conditionally by Cre recombinase (Xiao et al, Nature Immunology, 9:405-14, 2008). The mice were crossed to CD19-Cre mice to turn on the transgene expression specifically in B cells. Follicular B(FoB) cells were purified from CD19-Cre;miR-17~92 Tg/Tg mice (FoBtg1, FoBtg2, FoBtg3) and miR-17~92 Tg/Tg mice (FoBwt1, FoBwt2, FoBwt3) by MACS depletion of cells positive for CD5, CD43, and CD93 (also known as AA4.1). The purity of follicular B cells was examined by flow cytometry and was greater than 95% for all samples. Total RNA was extracted using RNeasy kit (QIAGEN).

2011-07-21 | E-GEOD-30877 | biostudies-arrayexpress

Follicular B (FoB) cells purified from miR-17-92 tKO mice

Project description:We have generated a miR-17~92 fl/fl allele whose expression can be turned off conditionally by Cre recombinase in the miR-106a-363-/-;miR-106b-25-/- background. The mice were crossed to CD19-Cre mice to turn off the expression of miR-17~92 specifically in B cells. Follicular B(FoB) cells were purified from CD19-Cre;miR-17~92 fl/fl;miR-106a-363;miR-106b~25 mice (tKO1, tKO2, tKO3) and CD19-cre (Control1, Control2, Control3) by MACS depletion of cells positive for CD9, CD43, and CD93 (also known as AA4.1). The purity of follicular B cells was examined by flow cytometry and was greater than 95% for all samples. Total RNA was extracted using RNeasy kit (QIAGEN).

2014-04-01 | E-GEOD-56376 | biostudies-arrayexpress

Follicular regulatory T cells control humoral and allergic immunity by restraining early B cell responses

Project description:Follicular regulatory T cells control humoral and allergic immunity by restraining early B cell responses

| PRJNA554101 | ENA