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MicroRNA-seq of Kynurenine stimulated mouse spleenocyte in vitro

ABSTRACT: microRNA-seq of Kynurenine stimulated mouse spleenocyte in vitro

PROVIDER: PRJNA689826 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13362205.fastq.gz	Fastqsanger.gz
	SRR13362206.fastq.gz	Fastqsanger.gz
	SRR13362207.fastq.gz	Fastqsanger.gz
	SRR13362208.fastq.gz	Fastqsanger.gz
	SRR13362209.fastq.gz	Fastqsanger.gz

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RNA-seq of Kynurenine stimulated mouse splenocyte in vitro

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microRNA-seq of Kynurenine stimulated mouse spleenocyte in vitro

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Project description:RNA-seq technology was conﬁrmed that mRNA and LncRNA expression have an important role in vaccine adjuvant in vivo and in vitro. Kynurenin, as an immunosuppressive adjuvant, but the exact mechanism of action with immune cells is still poorly understood. In the present study, mRNA and lncRNA sequencing was performed in mouse splenocytes stimulated by Kynurenin. These data provide an important basis for understanding the mechanisms underlying Kyn as an immunosuppressive adjuvant regulated the immune response.

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The aryl hydrocarbon receptor binds to kynurenine and mediates a signal supports the undifferentiated state in pluripotent stem cells

Project description:Kynurenine is generated from tryptophan by indoleamine 2,3-dioxygenase (IDO1) and binds to the aryl hydrocarbon receptor (AhR). We found that kynurenine generated by human embryonic stem cells (hESCs) and induced pluripotent stem cells (iPSCs) stimulated the AhR to bind selectively to the promoters and enhancers of self-renewal genes, thus enhancing their transcription. The kynurenine-AhR complex also directly stimulated the expression of IDO1 and AHR, activating a positive feedback loop. Substantial amounts of kynurenine that were not complexed with AhR were present in the culture medium, providing a paracrine signal for maintenance of the undifferentiated state. Kynurenine was not present in the medium of differentiated ESCs and iPSCs. When cells were induced to undergo ectodermal differentiation, the abundance of kynurenine in the medium was reduced through activation of the main kynurenine catabolic pathway mediated by aminotransferase 2 (KAT2), resulting in the secretion of 2-aminoadipic acid (2-AAA) into the culture medium. Thus, kynurenine in the culture medium is a biomarker for the undifferentiated state, and 2-AAA in the culture medium is a biomarker for ESCs and iPSCs that have committed to differentiate along the ectoderm lineage.

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Project description:Metabolic deregulation and immune escape are pivotal hallmarks of cancer; however, the profile of metabolic reprogramming in oral squamous cell carcinoma (OSCC) and how it drives immune escape remain unclear. We identified significant metabolic disorders in OSCC. Amino acid metabolism, especially tryptophan/kynurenine metabolism, was altered. Here, we found that kynurenine promotes migration, invasion, and proliferation in vitro and in vivo. In addition, most immune checkpoints were upregulated in patients with high kynurenine levels. We then identified that kynurenine can promote Siglec-15 expression via AhR activation. Furthermore, tumor-derived kynurenine can directly exhaust CD8+ T cells, whereas blocking of kynurenine transporters reversed this effect. Moreover, we found that ectopic expression of Siglec-15 can promote immune escape in tumor microenvironment (TME) by suppressing T cell infiltration and inducing CD8+ T cell exhaustion in vivo, while targeting AhR reduces kynurenine-mediated immune escape. Finally, we design NH2-MSNs nanoparticles to deliver Siglec-15 small interfering RNA, which successfully remodels the TME and enhances anti-PD-1 efficacy in tumor-bearing immunocompetent mice. Clinically, Siglec-15 expression is correlated with AhR expression and high infiltration of exhausted CD8+ T cells. These findings reveal that the Kyn/AhR/Siglec-15 signaling pathway is a novel immunometabolism mechanism in OSCC, thus opening a new therapeutic avenue for metabolic immunotherapy.

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