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

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

PROVIDER: PRJNA796517 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17578400.fastq.gz	Fastqsanger.gz
	SRR17578400_1.fastq.gz	Fastqsanger.gz
	SRR17578400_2.fastq.gz	Fastqsanger.gz
	SRR17578401.fastq.gz	Fastqsanger.gz
	SRR17578401_1.fastq.gz	Fastqsanger.gz

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

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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

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.

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Compare gene expression profiles of TCR transgenic CD4+ T helper type 1 (Th1) vs. type 17 (Th17) cells optimally stimulated by antigen and differentiated under Th1 or Th17 conditions.

Project description:The comparison of Th1 vs. Th17 cell expression profile has been plagued by 1) rarely use of physiologically relevant antigen-driven T helper cell differentiation; and 2) cell lineage tracking system to enrich highly pure Th subsets. We began our attempt to produce large numbers of antigen-specific T helper subsets for expression profiling, when Foxp3GFP knockin mice were first made by our laboratory in 2005. We crossed this line with syngeneic TEa TCR transgenic mice in C57BL/6 background, and use FACS to sort optimally stimulated, highly pure GFP(Foxp3)-negative populations for Th1 vs. Th17 expression profile comparison.

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Project description:T helper 17 (Th17) cells are a distinct subset of CD4+ T cells necessary for maintaining gut homeostasis and have prominent roles in autoimmunity and inflammation. Th17 cells have unique metabolic features, including a stem cell-like signature and reliance on mitochondrial respiratory chain function and tricarboxylic acid (TCA) cycle to coordinate metabolic and epigenetic remodeling. Dynamic changes in mitochondrial membrane morphology are key to sustain organelle function. However, it remains unclear whether mitochondrial membrane remodeling orchestrates metabolic and differentiation events in Th17 cells. Here we demonstrate that mitochondrial membrane fusion and tight cristae organization are required for Th17 cell function (i.e. cytokine expression). As a genetic model system we employ Th17 specific deletion of optic atrophy 1 (OPA1), a gene that encodes a protein involved in mitochondrial inner membrane fusion and cristae organization. As a result, we find that Th17 cells rely on mitochondrial fusion (due to their low metabolic activity). Here, we carry out DIA-based differential quantitative proteomic analysis of murine wild-type and OPA1 knock-out Th17 cells. Through Ingenuity pathway analysis and together with transcriptional and metabolomic profiling we identify the serine/threonine kinase liver associated kinase B1 (LKB1/STK11) as an essential node coupling mitochondrial function to IL-17A cytokine expression in T cells.

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Project description:Glioblastoma (GBM) remains a challenging malignancy with dismal prognoses despite aggressive treatment regimens. Intratumoral heterogeneity contributes to therapeutic resistance, with roles for stem cell-like brain tumor initiating cells (GBMs), glioma associated macrophages (GAMs), and communication between them. GAMs are derived from infiltrating lymphocytes, and monocyte migration is increased by GBM cell release of extracellular vesicles, including exosomes. GBM survival is promoted by the glucose transporter GLUT3, which was recently shown to alter macrophage activation states. We found that GBM-derived exosomes contain GLUT3 and that exosomes from GLUT3 expressing GBMs significantly increased monocyte migration in comparison to controls. Monocytes transfected with GLUT3 (but not GLUT1) also had significantly increased migration, demonstrating a direct role for GLUT3 in monocytes migration. Analysis of the transcriptome of exosome treated monocytes demonstrated that exosomes derived from GLUT3 expressing GBMs increasedGDF-15in monocytes. GDF-15 is a known regulator of monocyte migration, and we determined that knockdown of GDF-15 blocked the migration induced by GBM-derived exosomes. As GDF-15 induced monocyte migration is thought to involve MMP12, we next evaluated MMP12 as a potential mediator of the pro-migratory phenotype.MMP12was significantly increased in monocytes upon treatment with exosomes derived from GLUT3 expressing GBMs as was MMP12 activity. Together, our findings suggest a novel mechanism by which GBMs facilitate immune evasion and tumor progression: GBM-derived exosomes transfer GLUT3 to monocytes to increase a GDF-15/MMP12 pathway that promotes monocyte migration. The data also highlight the importance of understanding and targeting cell-cell interactions to improve glioblastoma treatment.

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