Tbet vs Eomes [RNA-Seq]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA706663 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13857831.fastq.gz | Fastqsanger.gz | |||
| SRR13857832.fastq.gz | Fastqsanger.gz | |||
| SRR13857833.fastq.gz | Fastqsanger.gz | |||
| SRR13857834.fastq.gz | Fastqsanger.gz | |||
| SRR13857835.fastq.gz | Fastqsanger.gz |
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Project description:T-bet and Eomes are related T-box transcription factors that control NK cell development. This study was designed to understand the specific roles of Eomes and T-bet in regulating gene expression. RNAseq data were generated for immature (CD11b- CD27+) and mature (CD11b+ CD27-) NK cells from T-bet KO (Tbet Ho) or control mice (Tbet WT) or from Eomes KO (Eomes Ho) or control mice (NK-Cre). Three samples were generated for each condition (Tri 1, 2, 3).
2021-05-10 | GSE168240 | GEO
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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Project description:Inflammatory (B220+ CD19+ CD44+ CD11c+ Tbet-AmCyanhi) B cells were sorted from female Tbet-AmCyan reporter mice at day 8, 10, and 15 post infection with LCMV-Armstrong. RNA-seq was employed to assess transcriptional changes in inflammatory B cells throughout the infection.
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Project description:Inflammatory (B220+ CD19+ CD44+ CD11c+ Tbet-AmCyanhi) B cells were sorted from female Tbet-AmCyan reporter mice at day 8, 10, and 15 post infection with LCMV-Armstrong. RNA-seq was employed to assess transcriptional changes in inflammatory B cells throughout the infection.
2022-01-27 | GSE192765 | GEO
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:This SuperSeries is composed of the SubSeries listed below.
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Project description:To gain mechanistic insights into how EOMES regulates CD4+ T-cell differentiation and function, we performed an RNA-seq analysis using Eomes-GFP reporter mice (Eomes+/GFP) to isolate GFP+ (EOMES+) and GFP- (EOMES-) CD4+ T-cells by FACS sorting. We also sequenced RNA from Eomes-deficient GFP+ and GFP- CD4+ T-cells isolated from EomesΔT/GFP knock-out mice, in which one Eomes allele is disrupted by GFP insertion and the DNA-binding domain of the other allele is deleted in T cells by Lck-driven Cre recombinase. Hence, we had two populations of GFP+ cells where the EOMES locus was transcribed, one with a transcriptionally active EOMES protein (Eomes+/GFP) and another one with no transcriptionally active EOMES (EomesΔT/GFP), plus the respective GFP-negative controls isolated from the same mice. A homogeneous population of EOMES-expressing CD4+ T cells were obtained by transferring naïve sorted CD25- CD45RBhigh CD4+ T-cells isolated from Eomes+/GFP reporter or EomesΔT/GFP knock-out donor animals into Rag2-/- mice. After three weeks of adoptive transfer GFP+ and GFP- CD4+ T-cell populations from these mice were FACS-sorted for transcriptome analysis by RNA sequencing.
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