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

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

PROVIDER: PRJNA817804 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18362963.fastq.gz	Fastqsanger.gz
	SRR18362964.fastq.gz	Fastqsanger.gz
	SRR18362965.fastq.gz	Fastqsanger.gz
	SRR18362966.fastq.gz	Fastqsanger.gz
	SRR18362967.fastq.gz	Fastqsanger.gz

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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: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]

2022-03-31 | GSE171675 | GEO

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

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

| PRJNA721880 | ENA

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

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

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Atovaquone-induced oxidative stress activates pentose phosphate pathway and immunogenic cell death in ovarian cancer

Project description:Atovaquone-induced oxidative stress activates pentose phosphate pathway and immunogenic cell death in ovarian cancer

| PRJNA1216615 | ENA

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]

| PRJNA721882 | ENA

High concentration of prolactin induce oxidative stress in ovine ovarian GCs by the pentose phosphate pathway through regulating the ROS and mitophagy pathways

Project description:High concentration of prolactin induce oxidative stress in ovine ovarian GCs by the pentose phosphate pathway through regulating the ROS and mitophagy pathways.

2022-10-23 | PXD037645 |

Atovaquone-induced oxidative stress activates pentose phosphate pathway and immunogenic cell death in ovarian cancer

Project description:Atovaquone, an FDA-approved oxidative phosphorylation (OXPHOS) inhibitor, has shown promise in treating epithelial ovarian cancer (EOC), the deadliest gynecologic malignancy. However, the precise mechanisms underlying its antitumorigenic effects remain unclear. We employed a longitudinal transcriptomic approach to characterize the molecular effects of atovaquone on EOC cells. Our findings demonstrate that atovaquone disrupts cellular homeostasis and metabolism, activates stress responses, and primes immune recognition. We observed temporal downregulation of genes and pathways involved in key cellular processes, such as cell cycle and DNA replication, correlating with reduced proliferative capacity. Atovaquone also downregulated both OXPHOS and glycolysis, while upregulating the pentose phosphate pathway, suggesting a metabolic shift toward redox homeostasis restoration in response to severe oxidative stress. Consistent with oxidative stress, we found that atovaquone activated endoplasmic reticulum (ER) stress, which is linked to immunogenic cell death. During ER stress, calreticulin, a Damage-Associated Molecular Pattern (DAMP), translocates to the plasma membrane, where it promotes immune recognition. We observed that calreticulin was upregulated on the plasma membrane of atovaquone-treated EOC cells. Additionally, we detected increased levels of other DAMPs, such as High Mobility Group Box 1 (HMGB1) and Mitochondrial Transcription Factor A (TFAM), in the supernatant of atovaquone-treated cells, indicating the release of immunogenic molecules. Moreover, increased expression of ligands for activating receptors of NK cells was observed and co-culture experiments showed enhanced NK cell activity toward atovaquone-treated cells. These results highlight atovaquone’s potential as an adjuvant therapy that activates immune responses, offering a new avenue for combination therapies in EOC treatment.

2025-02-02 | GSE288243 | GEO

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