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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.

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

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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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Project description:Metabolic pathways are now considered as intrinsic virulence attributes of pathogenic bacteria and hence represent potential targets for anti-bacterial strategies. Here, we addressed the role of the pentose phosphate pathway (PPP) and its connections with other metabolic pathways in the pathophysiology of Francisella novicida. We have previously shown that this intracellular bacterial pathogen used gluconeogenesis to metabolize host-derived nutrients in the cytosolic compartment of infected macrophages. Francisella species, which lacks the oxidative branch of the PPP, are equipped with all the genes of the non-oxidative branch (i.e. tktA, tal, rpiA and rpe, encoding transketolase, transaldolase, ribose-phosphate isomerase and ribulose phosphate epimerase, respectively). The involvement of the PPP in the early stage of intracellular life cycle of F. novicida was first demonstrated with the study of PPP inactivation mutants. Indeed, inactivation of tktA, rpiA or rpe genes, severely impaired intramacrophagic multiplication during the first 24–hours. However, time-lapse video microscopy demonstrated that rpiA and rpe mutants were able to resume late intracellular bacterial multiplication. To get further insight into the links between the PPP and other metabolic networks of the bacterium, we next performed a thorough proteo-metabolomic analysis of these mutants. We show that the PPP constitutes a major bacterial metabolic hub with multiple connections with glycolysis, tricarboxylic acid cycle and other metabolic pathways, such as fatty acid degradation and sulfur metabolism. Hence, our study highlights how, by its multiple connections with other metabolic pathways, PPP is instrumental to Francisella pathogenesis and growth in its intracellular niche.

2021-07-27 | PXD023550 | Pride

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