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Single-cell RNA-Seq analysis of WT and Bach2-deficient Foxp3+ Treg cells

ABSTRACT: Single-cell RNA-Seq analysis of WT and Bach2-deficient Foxp3+ Treg cells

PROVIDER: PRJNA527355 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8757410.fastq.gz	Fastqsanger.gz
	SRR8757420.fastq.gz	Fastqsanger.gz
	SRR8757430.fastq.gz	Fastqsanger.gz
	SRR8757440.fastq.gz	Fastqsanger.gz
	SRR8757450.fastq.gz	Fastqsanger.gz

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Bulk RNA-Seq analysis of WT and Bach2-deficient Foxp3+ Treg cells

Project description:These are the FastQ files used for the RNA-seq analysis of WT and Bach2-deficient splenic Foxp3+ Treg cells.

2020-05-12 | GSE127699 | GEO

Single-cell RNA-Seq analysis of WT and Bach2-deficient Foxp3+ Treg cells

Project description:These are the FastQ files used for scRNA-Seq analysis of WT and Bach2-deficient splenic Foxp3+ Treg cells

2020-05-12 | GSE128175 | GEO

Bulk RNA-Seq analysis of WT and Bach2-deficient Foxp3+ Treg cells

Project description:Bulk RNA-Seq analysis of WT and Bach2-deficient Foxp3+ Treg cells

| PRJNA527353 | ENA

Gene expression profiles of Foxp3RFP (WT), Foxp3∆EGFPiCre (Foxp3-deficient) and Foxp3∆EGFPiCreRictor∆/∆ (Foxp3-deficient and Rictor deficient) Treg cells.

Project description:Comparaison of the transcriptomes of WT and Foxp3-deficient regulatory T cells from the spleen of females that carried one mutant Foxp3∆EGFPiCre allele and a second competent Foxp3 allele (Foxp3RFP) that also directed the expression of the red fluorescent protein (RFP) . We then extended these studies to elucidate transcriptional pathways altered upon Rictor deletion in ∆Treg cells that may contribute to their improved regulatory function by analyzing the transcriptome of ∆Treg cells isolated from Foxp3∆EGFPiCre/+Rictor∆/∆ females.

2019-04-08 | GSE129472 | GEO

Gene expression profiles of Foxp3RFP (WT), Foxp3∆EGFPiCre (Foxp3-deficient) and Foxp3∆EGFPiCreRictor∆/∆ (Foxp3-deficient and Rictor deficient) Treg cells.

Project description:Gene expression profiles of Foxp3RFP (WT), Foxp3∆EGFPiCre (Foxp3-deficient) and Foxp3∆EGFPiCreRictor∆/∆ (Foxp3-deficient and Rictor deficient) Treg cells.

| PRJNA531459 | ENA

mRNA expression in CD4+ CD25+ GITR+ regulatory T cells from WT and Bach2 KO mice

Project description:Bach2 regulates homeostasis of foxp3+ regulatory T cells and protects against fatal lung disease in mice. Cells from WT and Bach2 KO spleen were isolated. CD4+ CD25+ GITR+ (Treg) cells were sorted by FACS sorting. Total RNAs were extracted from sorted Treg cells using by Rneasy Kit (Qiagen).

2013-11-14 | E-GEOD-52337 | biostudies-arrayexpress

Bach2 represses effector programmes to stabilize Treg-mediated immune homeostasis

Project description:Through their functional diversification, CD4+ T cells play key roles in both driving and constraining immune-mediated pathology. Transcription factors are critical in the generation and maintenance of cellular diversity and negative regulators antagonistic to alternate fates often act in conjunction with positive regulators to stabilize lineage specification1. Polymorphisms within the locus encoding a transcription factor BACH2 are associated with diverse immune-mediated diseases including asthma2, multiple sclerosis3, Crohn¹s disease4-5, coeliac disease6, vitiligo7 and type 1 diabetes8. A role for Bach2 in maintaining immune homeostasis, however, has not been established. Here, we define Bach2 as a broad regulator of immune activation that stabilizes immunoregulatory capacity while repressing the differentiation programmes of multiple effector lineages in CD4+ T cells. Bach2 was required for efficient formation of regulatory (Treg) cells and consequently for suppression of lethal inflammation in a manner that was Treg cell dependent. Assessment of the genome-wide function of Bach2, however, revealed that it represses genes associated with effector cell differentiation. Consequently, its absence during Treg polarization resulted in inappropriate diversion to effector lineages. In addition, Bach2 constrained full effector differentiation within Th1, Th2 and Th17 cell lineages. These findings identify Bach2 as a key regulator of CD4+ T-cell differentiation that prevents inflammatory disease by controlling the balance between tolerance and immunity. The role of Bach2t to regulate immune homeostasis was investigated by mapping DNA binding profiles of Bach2 in iTreg condition. The function of Bach2 was also evaluated by comparing transcriptome in WT and Bach2-deficient iTreg cells and further comparison was done with transcriptome in naive, Th1, Th2, and Th17 conditions.

2013-06-27 | E-GEOD-45975 | biostudies-arrayexpress

Transcription profile of WT and LKB1 (encoded by the gene Stk11)-deficient Treg cells

Project description:LKB1 deficiency in Treg cells impairs their survival, metabolism and suppressive function. To exclude the impact of excessive inflammation on LKB1-deficient Treg cells, we generated mixed bone marrow (BM) chimeras using Foxp3-Cre WT and Foxp3-Cre Stk11 fl/fl BM cells, together with CD45.1+ BM cells. We used microarray to compare the global transcription profile of dornor-derived LKB1-deficient Tregs with WT counterparts.

2017-08-29 | GSE83088 | GEO

The transcription factor BACH2 is required to establish immunosuppression within tumors

Project description:Through a diversity of functional lineages, cells of the innate and adaptive immune system either drive or constrain immune reactions within tumors. Thus, while the immune system has a powerful ability to recognize and kill cancer cells, this function is often suppressed preventing clearance of disease. The transcription factor (TF) BACH2 controls the differentiation and function of multiple innate and adaptive immune lineages, but its role in regulating tumor immunity is not known. Here, we demonstrate that BACH2 is required to establish immunosuppression within tumors. We found that growth of subcutaneously implanted tumors was markedly impaired in Bach2-deficient mice and coincided with intratumoral activation of both innate and adaptive immunity but was dependent upon adaptive immunity. Analysis of tumor-infiltrating lymphocytes in Bach2-deficient mice revealed high frequencies of CD4+ and CD8+ effector cells expressing the inflammatory cytokine IFN-Î³. Lymphocyte activation coincided with reduction in the frequency of intratumoral CD4+ Foxp3+ regulatory T (Treg) cells. Mechanistically, Treg-dependent inhibition of CD8+ T cells was required for BACH2-mediated tumor immunosuppression. These findings demonstrate that BACH2 is a key component of the molecular programme of tumor immunosuppression and identify a new target for development of therapies aimed at reversing immunosuppression in cancer. Analysis of tumor-infiltrating lymphocytes in Bach2-deficient mice revealed high frequencies of CD4+ and CD8+ effector cells expressing the inflammatory cytokine IFN-Î³. Lymphocyte activation coincided with reduction in the frequency of intratumoral CD4+ Foxp3+ regulatory T (Treg) cells. Mechanistically, Treg-dependent inhibition of CD8+ T cells was required for BACH2-mediated tumor immunosuppression.

2016-06-01 | E-GEOD-74653 | biostudies-arrayexpress

Gene expression in Bach2-deficient and wildtype CD4 single-positive thymocytes from mixed chimeric animals

Project description:The role of FoxP3+ regulatory T (Treg) cells in the maintenance of immunological tolerance is well established. Recently, genome-wide association studies (GWAS) in humans have associated polymorphisms within the BACH2 locus encoding the transcription factor BTB and CNC homology 1, basic leucine zipper transcription factor 2 (Bach2) with diverse allergic and autoimmune diseases including asthma, multiple sclerosis, Crohn's disease, celiac disease, generalized vitiligo and type 1 diabetes. Common to these diseases is a failure to adequately maintain immunological tolerance. However, a role for Bach2 in this process has not been established. Here, by assessing the phenotype of mice in which the Bach2 gene is disrupted, we demonstrate a non-redundant role for Bach2 in the prevention of a spontaneous lethal inflammatory disorder predominantly affecting the lung and gut with excessive T helper 2 (Th2) responses and formation of circulating autoantibodies. Bach2 was necessary for efficient induction of FoxP3 expression both during thymopoesis and upon stimulation of naïve peripheral CD4+ T cells under Treg polarizing conditions in vitro. Consequently, in bone marrow reconstitution experiments, Bach2 expression within the haematopoetic system was necessary for suppression of lethal autoimmunity in a manner that was FoxP3 dependent. These findings demonstrate a requirement for Bach2 in early lineage commitment of both thymic and induced Treg cells and point to shared mechanisms that underlie diverse allergic and autoimmune disorders that may serve as targets in the development of novel therapeutic strategies. Six samples were collected from separate mice: three Ly5.1+ wildtype thymocyte samples (biological replicates) and three Ly5.1- Bach2 knockout thymocyte samples (biological replicates).

2013-11-01 | E-GEOD-42598 | biostudies-arrayexpress

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