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RNA-seq of wild type and GLUT3-deficient T helper 17 (Th17) cells

ABSTRACT: RNA-seq of wild type and GLUT3-deficient T helper 17 (Th17) cells

PROVIDER: PRJNA792573 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17335145.fastq.gz	Fastqsanger.gz
	SRR17335146.fastq.gz	Fastqsanger.gz
	SRR17335147.fastq.gz	Fastqsanger.gz
	SRR17335148.fastq.gz	Fastqsanger.gz
	SRR17335149.fastq.gz	Fastqsanger.gz

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messengerRNA-seq of wild type, GLUT3-deficient and ACLY-deficient T helper 17 (Th17) cells

Project description:messengerRNA-seq of wild type, GLUT3-deficient and ACLY-deficient T helper 17 (Th17) cells

| PRJNA792580 | ENA

Histone H3 K9/14 acetylation of wild type and GLUT3-deficient T helper 17 (Th17) cells

Project description:Histone H3 K9/14 acetylation of wild type and GLUT3-deficient T helper 17 (Th17) cells

| PRJNA796517 | ENA

CIP2A negatively regulates Th17 differentiation

Project description:Interleukin 17 (IL-17) producing T helper 17 (Th17) cells are critical drivers of pathogenesis in a variety of autoimmune and inflammatory diseases. Strategies to mitigate excessive Th17 response thus remain an attractive target for immunotherapies. Here we report that Cancerous Inhibitor of Protein Phosphatase 2A (CIP2A) regulates IL-17 production by Th17 cells in human and mouse. Using CIP2A knock-out (KO) mice and siRNA-mediated CIP2A silencing in human primary CD4+ T cells, we demonstrated that CIP2A silencing results in a significant increase in IL-17 production. Interestingly, CIP2A deficient Th17 cells were characterized by increased strength and duration of STAT3 (Y705) phosphorylation. Genome-wide gene expression profile as well as the p-STAT3 (Y705) interactome of CIP2A deficient Th17 cells identified that CIP2A regulates the strength of the interaction between Acylglycerol kinase (AGK) and STAT3, and thereby, modulates STAT3 phosphorylation as well as expression of IL-17 in Th17 cells. Our results uncover the physiological function of CIP2A in Th17 cells and provides new opportunities for therapeutic intervention in Th17 cell mediated diseases.

2020-05-26 | PXD010612 | Pride

RNA-seq of wild type and GLUT3-deficient T helper 17 (Th17) cells

Project description:RNA-sequencing and analysis of in vitro differentiated Th1 and Th17 cells isolated from WT and Slc2a3-fl/fl Cd4-cre mice.

2022-02-13 | GSE192659 | GEO

messengerRNA-seq of wild type, GLUT3-deficient and ACLY-deficient T helper 17 (Th17) cells

Project description:messengerRNA-sequencing and analysis of in vitro differentiated Th17 cells isolated from WT, Slc2a3-fl/fl Cd4-cre or Acöy-fl/fl Cd4-cre mice in the presence or absence of 20 mM acetate for 24h.

2022-02-13 | GSE192663 | GEO

Histone H3 K9/14 acetylation of wild type and GLUT3-deficient T helper 17 (Th17) cells

Project description:Examination of histone acetlytion in Th17 cells

2022-02-13 | GSE193515 | GEO

Retinal pigment epithelial cells suppress interleukin-17-producing T-helper 17 cells

Project description:T cells that encounter cultured ocular pigment epithelial cells in vitro are inhibited from undergoing T cell receptor-triggered activation. Because retinal pigment epithelial (RPE) cells are able to suppress T-cell activation, we studied whether RPE cells could suppress cytokine production by activated T helper (Th) cells. In this study we showed that primary cultured RPE cells greatly suppressed activation of bystander CD4+ T cells in vitro, especially the cytokine production by the target T helper cells (Th1 cells, Th2 cells, Th17 cells, but not Th3 cells). Cultured RPE cells and RPE-supernatants significantly suppressed IL-17 producing CD4+ T cells, and RPE cells fully suppressed polarized Th17 cell lines that induced by recombinant proteins, IL-6 and TGFb2. Moreover, RPE cells failed to suppress IL-17 producing T cells in the presence of rIL-6. In addition, Th17 cells exposed to RPE were suppressed via TGFb, which produce RPE cells. These results indicate that retinal PE cells have immunosuppressive capacity in order to inhibit Th17-type effector T cells. Thus, ocular resident cells play a role in establishing immune regulation in the eye. Retinal pigment epithelium suppresses Th17 cells

2012-07-11 | E-GEOD-22877 | biostudies-arrayexpress

Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type, DDX5 knockout, RORc knockout, RmrpG262T knockin T helper 17 cell Transcriptomes [RNA-seq]

Project description:Purpose: The goals of this study are to compare in vitro polarized T helper 17 cell transcriptome profiling (RNA-seq) in different genetic background. Methods: Th17 mRNA profiles of 96hrs in vitro cultured T helper 17 cells from wild-type and mutant mice were generated by deep sequencing, using Illumina RapidRun. The sequence reads that passed quality filters were analyzed at the transcript isoform level with two methods: BurrowsâWheeler Aligner (BWA) and TopHat followed by CuffDiff. qRTâPCR validation was performed using SYBR Green assays. Results: Among the 325 genes that were significantly dysregulated in DDX5-deficient T cells, approximately 40% were previously identified as RORÎ³t targets in Th17 cells. 96 RORÎ³t-dependent Th17 cell genes co-regulated by Rmrp together with DDX5. Conclusions: Our study suggest that the DDX5-Rmrp axis is critical for expression of a critical subset of the RORÎ³t transcriptional targets in Th17 cells. mRNA profiles of 96hr in vitro cultured Th17 from wild type (WT) and mutant mice were generated by deep sequencing using Illumina RapidRun.

2015-12-21 | E-GEOD-70108 | biostudies-arrayexpress

Retinal pigment epithelial cells suppress interleukin-17-producing T-helper 17 cells

2012-07-12 | GSE22877 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type, DDX5 knockout, RORc knockout, RmrpG262T knockin T helper 17 cell Transcriptomes [RNA-seq]

Project description:Purpose: The goals of this study are to compare in vitro polarized T helper 17 cell transcriptome profiling (RNA-seq) in different genetic background. Methods: Th17 mRNA profiles of 96hrs in vitro cultured T helper 17 cells from wild-type and mutant mice were generated by deep sequencing, using Illumina RapidRun. The sequence reads that passed quality filters were analyzed at the transcript isoform level with two methods: Burrows–Wheeler Aligner (BWA) and TopHat followed by CuffDiff. qRT–PCR validation was performed using SYBR Green assays. Results: Among the 325 genes that were significantly dysregulated in DDX5-deficient T cells, approximately 40% were previously identified as RORγt targets in Th17 cells. 96 RORγt-dependent Th17 cell genes co-regulated by Rmrp together with DDX5. Conclusions: Our study suggest that the DDX5-Rmrp axis is critical for expression of a critical subset of the RORγt transcriptional targets in Th17 cells.

2015-12-21 | GSE70108 | GEO

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