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Tbet dysregulation compensates for Ets-deficiency in iNKT1 cells

ABSTRACT: Tbet dysregulation compensates for Ets-deficiency in iNKT1 cells

PROVIDER: PRJNA1171809 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30951985.fastq.gz	Fastqsanger.gz
	SRR30951985_1.fastq.gz	Fastqsanger.gz
	SRR30951985_2.fastq.gz	Fastqsanger.gz
	SRR30951986_1.fastq.gz	Fastqsanger.gz
	SRR30951986_2.fastq.gz	Fastqsanger.gz

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Tbet dysregulation compensates for Ets-deficiency in iNKT1 cells

Project description:The goal of this study was to compare the gene expression program of liver iNKT1 cells from Control mice to those with a postselection deletion of the transcription factor Ets1 and heterozybous deletion of Tbx21. Ets1-floxed and Tbx21-floxed alleles were deleted in iNKT1 cells using Tbx21Cre bacterial artifical chromosome transgenic mice that also carry a Rosa26-floxed-stop-YFP reporter. Control iNKT1 cells were Tbx21Cre+ Rosa26-floxed-stop-YFP reporter+ and cKOHet iNKT cells were Tbx21Cre+ Ets1F/F Tbx21F/+ Rosa26-floxed-stop-YFP reporter+. The differentially expressed genes were compared to those in liver iNKT1 cells with postselection deletion of Ets1 only. We examined gene expression by RNA-sequencing of sorted iNKT1 cells (CD1d-Tet-PBS57+ YFP+) from the liver. Reads were aligned to the mm10 reference genome using Tophat v 2.1.0. Reads were assigned to genes using the htseq-count tool from HTSeq v 0.6.1 and gene annotations from Ensembl release 78. Differential expression was calculated across 3 independent replicates by EdgeR. We found that iNKT1 cells lacking Ets1 upregulated Tbx21 and its protein Tbet, many Tbet target genes, and CD8 effector T cell associated genes.

2024-10-16 | GSE279288 | GEO

Ets1 dampens expression of Tbet and CD8- or NK-like effector programing in postselection iNKT1 cells [scRNA-seq]

Project description:The goal of this study was to compare the gene expression program of thymic iNKT1 cells from Control mice to those with a postselection deletion of the transcription factor Ets1 at the single cell level. Ets1-floxed alleles were deleted in iNKT1 cells using Tbx21Cre bacterial artifical chromosome transgenic mice that also carry a Rosa26-floxed-stop-YFP reporter. Control iNKT1 cells were Tbx21Cre+ Rosa26-floxed-stop-YFP reporter+. We isolated all thymic YFP+ cells from Control and cKO mice and processed for scRNA-seq using the 10X Genomics Chromium. Data was processed using the Cell Ranger program for 10X Genomics. . We found that iNKT1 cells lacking Ets1 upregulated Tbx21 and its protein Tbet, many Tbet target genes, and CD8 effector T cell associated genes.

2024-10-10 | GSE278707 | GEO

Ets1 dampens expression of Tbet and CD8- or NK-like effector programing in postselection iNKT1 cells [RNA-seq]

Project description:The goal of this study was to compare the gene expression program of thymic and liver iNKT1 cells from Control mice to those with a postselection deletion of the transcription factor Ets1. Ets1-floxed alleles were deleted in iNKT1 cells using Tbx21Cre bacterial artifical chromosome transgenic mice that also carry a Rosa26-floxed-stop-YFP reporter. Control iNKT1 cells were Tbx21Cre+ Rosa26-floxed-stop-YFP reporter+. We examined gene expression by RNA-sequencing of sorted iNKT1 cells (CD1d-Tet-PBS57+ YFP+) from the thymus and liver. Reads were aligned to the mm10 reference genome using Tophat v 2.1.0. Reads were assigned to genes using the htseq-count tool from HTSeq v 0.6.1 and gene annotations from Ensembl release 78. Differential expression was calculated across 3 independent replicates by EdgeR. We found that iNKT1 cells lacking Ets1 upregulated Tbx21 and its protein Tbet, many Tbet target genes, and CD8 effector T cell associated genes.

2024-10-10 | GSE278708 | GEO

Tbet-Eomes

Project description:Tbet-Eomes

| PRJNA706657 | ENA

Expression data from Tbet+ and Tbet- Memory B cells

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. NaÃ¯ve, 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

2016-08-01 | E-GEOD-81189 | biostudies-arrayexpress

RNA-seq of Tgfbr2-deficient thymic iNKT1 cells

Project description:The goal of this study was to identify genes that are regulated by TGF-b-signaling in thymic iNKT1 cells. To specifically target Tgfbr2 deletion to iNKT1 cells we created Tbx21Cre bacterial artifical chromosome transgenic mice with a Rosa26-floxed-stop-YFP reporter and floxed alleles of Tgfbr2 . We examined gene expression by RNA-sequencing in sorted iNKT1 cells (CD1d-Tet-PBS57+ YFP+) from Ctrl (Tbx21Cre; Rosa26-YFP+) and cKO (Tbx21Cre; Rosa26-YFP+; Tgfbr2F/F) mice. Reads were aligned to the mm10 reference genome using STAR v2.5.2. Reads were assigned to genes using the htseq-count tool from HTSeq v 0.6.1 and gene annotations from Ensembl release 78. Differential expression was calculated across 3 independent replicates by EdgeR. We found that TGF-b was required for normal numbers of iNKT1 cells and induced a classic TGF-b gene program in thymic iNKT1 cells but did not regulate expression of Tbx21 (T-bet).

2022-10-13 | GSE215128 | GEO

Ets1 dampens expression of Tbet and CD8- or NK-like effector programing in postselection iNKT1 cells [scRNA-seq]

Project description:Ets1 dampens expression of Tbet and CD8- or NK-like effector programing in postselection iNKT1 cells [scRNA-seq]

| PRJNA1168495 | ENA

Ets1 dampens expression of Tbet and CD8- or NK-like effector programing in postselection iNKT1 cells [RNA-seq]

Project description:Ets1 dampens expression of Tbet and CD8- or NK-like effector programing in postselection iNKT1 cells [RNA-seq]

| PRJNA1168497 | ENA

RNA-seq of wild-type iNKT1 cells from thymus, liver and spleen

Project description:The goal of this study was to compare the gene expression program of iNKT1 cells in the thymus, liver and spleen. To identify iNKT1 cells we created Tbx21Cre bacterial artifical chromosome transgenic mice with a Rosa26-floxed-stop-YFP reporter. We examined gene expression by RNA-sequencing in sorted iNKT1 cells (CD1d-Tet-PBS57+ YFP+) from the thymus, liver and spleen. Reads were aligned to the mm10 reference genome using Tophat v 2.1.0. Reads were assigned to genes using the htseq-count tool from HTSeq v 0.6.1 and gene annotations from Ensembl release 78. Differential expression was calculated across 3 independent replicates by EdgeR. We found that iNKT1 cells from all tissues had very similar gene expression programs but that there were subtle difference in each tissue that may have relevance for survival and function in these tissues.

2022-10-15 | GSE215338 | GEO

Tbet regulates the accessible chromatin of Be1 B cells

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.

2019-04-29 | GSE118984 | GEO

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