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Double Negative T Cells Downregulate Intrahepatic Inflammation and Ameliorate Hepatic Ischemia and Reperfusion Injury via CD39-adenosinergic axis [ChIP-seq]

ABSTRACT: Double Negative T Cells Downregulate Intrahepatic Inflammation and Ameliorate Hepatic Ischemia and Reperfusion Injury via CD39-adenosinergic axis [ChIP-seq]

PROVIDER: PRJNA1032479 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26535408_1.fastq.gz	Fastqsanger.gz
	SRR26535408_2.fastq.gz	Fastqsanger.gz
	SRR26535409_1.fastq.gz	Fastqsanger.gz
	SRR26535409_2.fastq.gz	Fastqsanger.gz

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Double Negative T Cells Downregulate Intrahepatic Inflammation and Ameliorate Hepatic Ischemia and Reperfusion Injury via CD39-adenosinergic axis

Project description:Double Negative T Cells Downregulate Intrahepatic Inflammation and Ameliorate Hepatic Ischemia and Reperfusion Injury via CD39-adenosinergic axis

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Double Negative T Cells Downregulate Intrahepatic Inflammation and Ameliorate Hepatic Ischemia and Reperfusion Injury via CD39-adenosinergic axis [RNA-seq]

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Double Negative T Cells Downregulate Intrahepatic Inflammation and Ameliorate Hepatic Ischemia and Reperfusion Injury via CD39-adenosinergic axis [RNA-seq]

Project description:Converted double negative T cells (cDNT) highly express CD39 and hydrolyze ATP into adenosine. ATP/adenosine derived purinergic signaling plays a critical role in immune regulation. However, the role and mechanisms of ATP/adenosine in cDNT is unclear.

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Double Negative T Cells Downregulate Intrahepatic Inflammation and Ameliorate Hepatic Ischemia and Reperfusion Injury via CD39-adenosinergic axis [ChIP-seq]

Project description:Converted double negative T cells (cDNT) highly expressed ATP hydrolytic enzyme CD39 and hydrolyzed extracellular ATP (eATP) into adenosine. We found that adenosine upregulated the transcription factor FOXO1 expression in cDNT. CUT&Tag assay was performed to investigate the FOXO1 binding promoter sites in cDNT.

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Double Negative T Cells Downregulate Intrahepatic Inflammation and Ameliorate Hepatic Ischemia and Reperfusion Injury via CD39-adenosinergic axis

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