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Control of regulatory T cell function by the non-oxidative pentose phosphate pathway

ABSTRACT: Control of regulatory T cell function by the non-oxidative pentose phosphate pathway

PROVIDER: PRJNA721880 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14181749.fastq.gz	Fastqsanger.gz
	SRR14181750.fastq.gz	Fastqsanger.gz
	SRR14181751.fastq.gz	Fastqsanger.gz
	SRR14181752.fastq.gz	Fastqsanger.gz
	SRR14181753.fastq.gz	Fastqsanger.gz

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Control of regulatory T cell function by the non-oxidative pentose phosphate pathway [ATAC-seq]

Project description:Non-oxidative pentose phosphate pathway (PPP) is a crucial gatekeeper of glucose catabolism in metabolic tissues. However, its role in regulatory T cells (Tregs) remains unknown. Here we report deleting transketolase (TKT), an indispensable enzyme of non-oxidative PPP, in Tregs caused a fatal auto-immune disease in mice. TKT deletion impaired suppressive capability without disturbing Treg cell number. Mechanistically, TKT deficiency caused Treg metabolic remodeling with decreased glucose catabolism, activated fatty acid and amino acid catabolism and uncontrolled oxidative phosphorylation. Moreover, excessive ammonia from deregulated amino acid catabolism impaired mitochondrial fitness while reduced α-ketoglutarate/succinate ratio led to DNA hypermethylation, limiting functional gene expression and suppressive activity of TKT-deficient Tregs. Therefore, our study identifies non-oxidative PPP as a new pathway for controlling Treg function.

2022-03-31 | GSE172047 | GEO

Control of regulatory T cell function by the non-oxidative pentose phosphate pathway [RNA-Seq]

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Non-oxidative pentose phosphate pathway controls regulatory T cell function by integrating metabolism and epigenetics

Project description:Regulatory T cells (Tregs) are critical for maintaining immune homeostasis and preventing autoimmunity. Here, we show that the non-oxidative pentose phosphate pathway (PPP) regulates Treg function to prevent autoimmunity. Deletion of transketolase (TKT), an indispensable enzyme of non-oxidative PPP, in Tregs causes a fatal autoimmune disease in mice, with impaired Treg suppressive capability despite regular Treg numbers and normal Foxp3 expression levels. Mechanistically, reduced glycolysis and enhanced oxidative stress induced by TKT deficiency triggers excessive fatty acid and amino acid catabolism, resulting in uncontrolled oxidative phosphorylation and impaired mitochondrial fitness. Reduced -KG levels as a result of reductive TCA cycle activity leads to DNA hypermethylation, thereby limiting functional gene expression and suppressive activity of TKT-deficient Tregs. We also find that TKT levels are frequently downregulated in Tregs of patients with autoimmune disorders. Our study identifies the non-oxidative PPP as an integrator of metabolic and epigenetic processes that control Treg function.

2022-03-31 | GSE198995 | GEO

Control of regulatory T cell function by the non-oxidative pentose phosphate pathway [ATAC-seq]

Project description:Control of regulatory T cell function by the non-oxidative pentose phosphate pathway [ATAC-seq]

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Control of regulatory T cell function by the non-oxidative pentose phosphate pathway [RNA-Seq]

Project description:Control of regulatory T cell function by the non-oxidative pentose phosphate pathway [RNA-Seq]

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Non-oxidative pentose phosphate pathway controls regulatory T cell function by integrating metabolism and epigenetics

Project description:Non-oxidative pentose phosphate pathway controls regulatory T cell function by integrating metabolism and epigenetics

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Anaerobic fermentative metabolism of Corynebacterium glutamicum is hampered by a functional oxidative pentose phosphate pathway

Project description:Anaerobic fermentative metabolism of Corynebacterium glutamicum is hampered by a functional oxidative pentose phosphate pathway

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Progesterone increases metabolism via the pentose phosphate pathway in bovine uterine epithelial cells

Project description:During early pregnancy, glucose is essential for the uterine epithelium and the developing embryo. In cows, studies have shown that progesterone increases the secretion of glucose into the uterine lumen. Nevertheless, how progesterone affects glucose metabolism in the uterine epithelium has been sparsely investigated. Therefore, our objective was to investigate how progesterone influences glucose metabolism in immortalized bovine uterine epithelial (BUTE) cells. Progesterone treatment (10 μM) increased glucose consumption. To gain a more global picture of the effects of progesterone, RNAseq was performed after BUTE cells were treated with vehicle (DMSO) or 10 μM for 24 hours. KEGG analysis indicated that progesterone altered genes associated with metabolic pathways and glutathione metabolism. Manually examining genes unique to specific glucose metabolic pathways identified an increase in the rate-limiting enzyme in the pentose phosphate pathway—glucose-6-phosphate dehydrogenase. Functionally, a major product of the pentose phosphate pathway is NADPH, and progesterone treatment increased NADPH concentrations in BUTE cells. In cows, immunohistochemistry confirmed that glucose-6-phosphate dehydrogenase levels were higher in the uterine epithelium in the luteal phase when progesterone concentrations are high. In conclusion, progesterone increased glucose-6-phosphate dehydrogenase expression and metabolism via the pentose phosphate pathway in the bovine uterine epithelium. This metabolism could provide substrates for cell proliferation, molecules to be secreted into the uterine lumen that supports embryonic development, or maintain reduction/oxidation balance in the uterine epithelium.

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Project description:Metabolic reprogramming has emerged as a crucial regulator of immune cell activation but how systemic metabolism influences immune cell metabolism and function remains to be investigated. To investigate the effect of dyslipidemia on immune cell metabolism, we performed in-depth transcriptional, metabolic and functional characterization of macrophages isolated from hypercholesterolemic mice. Systemic metabolic changes in such mice alter cellular macrophage metabolism and attenuate inflammatory macrophage responses. In addition to diminished maximal mitochondrial respiration, hypercholesterolemia reduces the LPS-mediated induction of the pentose phosphate pathway (PPP) and the Nrf2-mediated oxidative stress response. Our observation that suppression of the PPP diminishes LPS-induced cytokine secretion supports the notion that this pathway contributes to inflammatory macrophage responses. Overall, this study reveals that systemic and cellular metabolism are strongly interconnected, together dictating macrophage phenotype and function.

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