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Ketogenesis activates metabolically protective γδ T cells in visceral adipose tissue

ABSTRACT: Ketogenesis activates metabolically protective γδ T cells in visceral adipose tissue

PROVIDER: PRJNA564510 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10084505.fastq.gz	Fastqsanger.gz
	SRR10084506.fastq.gz	Fastqsanger.gz
	SRR10084507.fastq.gz	Fastqsanger.gz
	SRR10084508.fastq.gz	Fastqsanger.gz
	SRR10084509.fastq.gz	Fastqsanger.gz

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Ketogenesis activates metabolically protective γδ T cells in visceral adipose tissue [scRNA-Seq]

Project description:Ketone bodies are essential alternative fuels that allow humans to survive periods of glucose scarcity induced by starvation and prolonged exercise. A widely used ketogenic diet (KD), that is extremely high in fat with very-low carbohydrates, drives the host into using β-hydroxybutyrate (BHB) for the production of ATP and lowers NLRP3-mediated inflammation. However, the extremely high fat composition of KD raises the question of how ketogenesis impacts adipose tissue to control inflammation and energy homeostasis. Using single-cell RNA sequencing of adipose tissue-resident immune cells, we identified that KD expands metabolically protective γδ T cells that restrain inflammation. However, a long-term KD caused obesity, impaired metabolic health and depleted the adipose resident γδ T cells. Moreover, mice lacking γδ T cells have impaired glucose homeostasis. We conclude that γδ T cells are mediators of protective immunometabolic responses that link fatty acid driven fuel utilization to reduced adipose tissue inflammation.

2019-09-10 | GSE137076 | GEO

Ketogenesis activates metabolically protective γδ T cells in visceral adipose tissue [scRNA-Seq]

Project description:Ketogenesis activates metabolically protective γδ T cells in visceral adipose tissue [scRNA-Seq]

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Ketogenesis activates metabolically protective γδ T cells in visceral adipose tissue [bulk RNA-Seq]

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Ketogenesis activates metabolically protective γδ T cells in visceral adipose tissue [bulk RNA-Seq]

Project description:Ketogenesis activates metabolically protective γδ T cells in visceral adipose tissue [bulk RNA-Seq]

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Ketogenesis activates metabolically protective γδ T cells in visceral adipose tissue.

Project description:Ketone bodies are essential alternative fuels that allow humans to survive periods of glucose scarcity induced by starvation and prolonged exercise. A widely used ketogenic diet (KD), which is extremely high in fat with very low carbohydrates, drives the host into using β-hydroxybutyrate for the production of ATP and lowers NLRP3-mediated inflammation. However, the extremely high fat composition of KD raises the question of how ketogenesis affects adipose tissue to control inflammation and energy homeostasis. Here, by using single-cell RNA sequencing of adipose-tissue-resident immune cells, we show that KD expands metabolically protective γδ T cells that restrain inflammation. Notably, long-term ad libitum KD feeding in mice causes obesity, impairs metabolic health and depletes the adipose-resident γδ T cells. In addition, mice lacking γδ T cells have impaired glucose homeostasis. Our results suggest that γδ T cells are mediators of protective immunometabolic responses that link fatty acid-driven fuel use to reduced adipose tissue inflammation.

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Ketogenesis activates metabolically protective γδ T cells in visceral adipose tissue

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-09-10 | GSE137077 | GEO

Ketogenic diet activates protective γδ T cell responses against influenza virus infection

Project description:Influenza A virus (IAV) infection-associated morbidity and mortality are a key global healthcare concern, necessitating the identification of novel therapies capable of reducing the severity of IAV infections. In this study, we show that the consumption of a low-carbohydrate, high-fat ketogenic diet (KD) protects mice from lethal IAV infection and disease. KD feeding resulted in an expansion of γδ T cells in the lung that improved barrier functions, thereby enhancing anti-viral resistance. Expansion of these protective γδ T cells required metabolic adaptation to a ketogenic diet, as neither feeding mice a high-fat high-carbohydrate diet nor providing chemical ketone body substrate that bypasses hepatic ketogenesis protected against infection. Therefore, KD mediated immune-metabolic integration represents a viable avenue towards preventing or alleviating influenza disease.

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Project description:Influenza infection causes high rates of hospitalization and mortality in infants. γδ T cells are critical for immune responses against pathogens as regulators and effectors, especially in infants, and yet the roles of neonatal γδ T cells in influenza remain to be investigated. Here we report that γδ T cells were protective against mortality associated with neonatal influenza infection. Infection induced the accumulation and activation of γδ T cells, which transiently expressed IL-17a to enhance early IL-33 production by lung epithelial cells via STAT3 phosphorylation. Subsequently, this led to type 2 immune responses with elicited infiltration of ILC2s and Tregs resulting in increased amphiregulin secretion and tissue repair. Loss of γδ T cells did not alter viral clearance or IFN-γ production. Thus, our results identify a specific requirement for γδ T cells in influenza-infected neonates by initiating type 2 immune responses, mediating tissue homeostasis, and promoting lung integrity.

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Ketogenic diet activates protective γδ T cell responses against influenza virus infection

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