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Next Generation Sequencing Facilitates Qunatitative Analysis of MondoA+/+Foxp3Cre and MondoAfl/flFoxp3Cre Treg cells Transcriptomes

ABSTRACT: Next Generation Sequencing Facilitates Qunatitative Analysis of MondoA+/+Foxp3Cre and MondoAfl/flFoxp3Cre Treg cells Transcriptomes

PROVIDER: PRJNA720935 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	SRR14198865.fastq.gz	Fastqsanger.gz
	SRR14198866.fastq.gz	Fastqsanger.gz
	SRR14198867.fastq.gz	Fastqsanger.gz
	SRR14198868.fastq.gz	Fastqsanger.gz

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Next Generation Sequencing Facilitates Qunatitative Analysis of MondoA+/+Foxp3Cre and MondoAfl/flFoxp3Cre Treg cells Transcriptomes

Project description:RNA-seq of Treg cells derived from MondoA+/+Foxp3Cre and MondoAfl/flFoxp3Cre mice.

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Next Generation Sequencing Facilitates Quantitative Analysis of adipose tissue Treg and LN Treg Transcriptomes

Project description:The goal of this study is to reveal unique features of adipose Tregs and to study mechanisms underlying how mediator Med23 regulate adipose Treg function in aged mice. Therefore, mRNA profiles of LN Tregs (from 4-month old Foxp3Cre mice) and adipose Tregs (from 4-month old Foxp3Cre, 4-month old obese Foxp3Cre, 10-month old Foxp3Cre and 10-month old Med23fl/fl;Foxp3Cre mice) were generated by deep sequencing, single experiment, using Illumina HiSeq2000. We compared transcriptome features between lymph node-derived Tregs and adipose Tregs from 4-month old lean or obese mice. Using unbiased comparative gene expression analyses, we found adipose Tregs display an up-signature of Insr (Insulin receptor) and Hif1a, while Pparg acts as a positive control. We next compared gene expression profiles of adipose Tregs from 10-month old Med23fl/fl;Foxp3Cre (MKO) and Foxp3Cre (WT) mice. adipose Med23-ΔTreg cells display impaired transcription of Pparg and Il1rl1 (ST2), and they simultaneously acquire the expression of Nt5e (CD73), while Entpd1 (CD39) expression was not dramatically altered. Our studies implicate protective roles of CD73hi adipose Tregs and offer new therapeutic strategies against age-associated metabolic syndrome.

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Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type and poh1-/- splenic foxp3＋Treg cells

Project description:Purpose: The goals of this study are to compare the transcriptome profiling of Wild Type and poh1-/- splenic foxp3＋Treg cells Methods:Splenic CD4+Foxp3+ (YFP+) cells mRNA profiles of 2-week-old poh1+/+ Foxp3Cre+ wild type and poh1fl/fl Foxp3Cre+ mice were generated by deep sequencing, using Illumina HiSeq 2500. The sequence reads that passed quality filters were analyzed with edgeR. qRT–PCR validation was performed using SYBR Green assays Results:Using an optimized data analysis workflow, we mapped about 50 million sequence reads per sample to the mouse genome (build mm10). Among all genes expressed, 1067 genes were upregulated and1391 genes were downregulated in poh1−/− Foxp3+ Treg cells relative to their expression in POH1 +/+ Treg cells. The gene-expression altered in POH1-ablated cells adversely correlated with those expressed in Treg cells in TCR-dependent manner. The gene sets were downreglated in POH1-deficiency Treg cells encoding various cell-surface receptors and intracellular molecules involved in migration, suppressive function and signature of Treg cells. Conclusions:Gene expression in POH1-deficiency Treg cells was markedly diverse compared with that in POH1-sufficient Treg cells.

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2021-07-15 | GSE152082 | GEO

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Project description:Regulatory T (Treg) cells harbor immune suppressive capacity and are crucial for the maintenance of peripheral tolerance. Treg cells are considered to be heterogenic, where compromised FOXP3 expression results in the generation of exTreg cells. Here we report that the E3 deubiquitinase USP21 prevents the depletion of FOXP3 protein and restricts tissue-resident exTreg cell generation. Mice lacking USP21 in Treg cells display immune disorders characterized by spontaneous T cell activation and excessive T helper type 1 (Th1) skewing. USP21 stabilizes FOXP3 protein by mediating its deubiquitination and therefore helps to maintain the expression of Treg signature genes. Moreover, at inflamed loci, tissue-resident USP21-deficient Treg cells display a Th1-like effector phenotype. Therefore, we demonstrate how USP21 controls the identity of tissue-resident Treg cells by preventing FOXP3 loss.

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Single-cell sequencing of wt and Rbx1-deficient Treg cells from mice

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