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Adenosinergic signaling alters natural killer cell functional responses

ABSTRACT: Adenosinergic signaling alters natural killer cell functional responses

PROVIDER: PRJNA490085 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7812590_1.fastq.gz	Fastqsanger.gz
	SRR7812590_2.fastq.gz	Fastqsanger.gz
	SRR7812591_1.fastq.gz	Fastqsanger.gz
	SRR7812591_2.fastq.gz	Fastqsanger.gz
	SRR7812592_1.fastq.gz	Fastqsanger.gz

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HIV/HBV co-infection remodels the immune landscape and Natural Killer cell functional responses

Project description:HIV/HBV co-infection remodels the immune landscape and Natural Killer cell functional responses

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Adenosinergic Signaling Alters Natural Killer Cell Functional Responses.

Project description:Adenosine is a potent immunosuppressive purine metabolite contributing to the pathogenesis of solid tumors. Extracellular adenosine signals on tumor-infiltrating NK cells to inhibit their proliferation, maturation, and cytotoxic function. Cytokine priming imparts upon NK cells distinct activation statuses, which modulate NK anti-tumor immunity and responses to purinergic metabolism. Here, for the first time, we investigated human NK cell responses to adenosinergic signaling in the context of distinct cytokine priming programs. NK cells were shown to be hyper-responsive to adenosine when primed with IL-12 and IL-15 compared to IL-2, exhibiting enhanced IFN-γ expression from CD56bright and CD56dim subsets while modulating the expression of activation marker NKG2D. These responses resulted in signaling that was dependent on mTOR. Adenosine induced upregulation of transcriptional signatures for genes involved in immune responses while downregulating cellular metabolism and other protein synthesis functions that correlate to inhibited oxidative phosphorylation and glycolysis. Overall, our findings show that adenosine acts on specific cellular pathways rather than inducing a broad inhibition of NK cell functions. These responses are dependent on cytokine priming signatures and are important in designing therapeutic interventions that can reprogram NK cell immunometabolism for improved immunotherapies of solid tumors.

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Project description:Innate immune responses rely on rapid and precise orchestration of gene regulation mediated by accessibility of regulatory regions to key transcription factors. However, the extent to which acute activation alters accessibility and the roles of distinct classes of transcription factors in this process are unsatisfactorily understood. Here, we investigated and integrated epigenomic modifications and transcriptomic changes occurring upon activation of natural killer (NK) cells.

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Adenosinergic signaling alters natural killer cell functional responses

Project description:Purpose: The goal of this study was to globally characterize the transcript levels of genes NK cells in the presence or absence of adenosine

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Project description:Background: Hepatitis B (HBV) and human immunodeficiency virus (HIV) co-infection is a common occurrence globally, with significant morbidity and mortality. Both viruses lead to dysregulated immune responses including changes in natural killer (NK) cells, a key component of antiviral defense and a promising target for HBV cure strategies. In this study we used high-throughput single cell analysis to explore the immune cell landscape in people with HBV mono-infection and HIV/HBV co-infection, on antiviral therapy, with emphasis on identifying the distinctive characteristics of NK cell subsets. Results: Our data show striking differences in the transcriptional programs of NK cells. HIV/HBV co-infection was characterized by an overrepresentation of adaptive, KLRC2 expressing NK cells, including a higher abundance of a chemokine enriched (CCL3/CCL4) adaptive cluster. The NK cell remodeling in HIV/HBV co-infection was reflected in enriched activation pathways shared with T cells, including CD3 phosphorylation and ZAP-70 translocation that can mediate stronger ADCC responses and a bias towards chemokine/cytokine signaling. By contrast HBV mono-infection imposed a stronger cytotoxic profile on NK cells and a more prominent signature of exhaustion with higher circulating levels of HBsAg. Mirroring the transcriptomic analysis, phenotypic alterations in the NK cell pool in co-infection were consistent with increased ‘adaptiveness’ and better capacity for ADCC compared to HBV mono-infection. Overall an adaptive NK cell signature correlated inversely with circulating levels of HBsAg and HBV-RNA in our cohort. Conlcusions: This study provides new insights into the differential transcriptional signature and functional profile of NK cells in HBV and HIV/HBV co-infection, highlighting new pathways that can be manipulated to tailor NK cell-focused approaches to advance cure strategies in the different population groups.

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