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Cholesterol mobilization regulates dendritic cell maturation and the immunogenic response to cancer

ABSTRACT: Cholesterol mobilization regulates dendritic cell maturation and the immunogenic response to cancer

PROVIDER: PRJNA1190849 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31513208.fastq.gz	Fastqsanger.gz
	SRR31513209.fastq.gz	Fastqsanger.gz
	SRR31513210.fastq.gz	Fastqsanger.gz
	SRR31513211.fastq.gz	Fastqsanger.gz
	SRR31513212.fastq.gz	Fastqsanger.gz

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Cholesterol mobilization regulates dendritic cell maturation and the immunogenic response to cancer

Project description:Maturation of conventional dendritic cells (cDCs) is crucial for maintaining tolerogenic safeguards against auto-immunity and for promoting immunogenic responses to pathogens and cancer. The subcellular mechanism for cDC maturation remains poorly defined. We show that cDCs mature by leveraging an internal reservoir of cholesterol – generated by de novo synthesis and recycled from extracellular cell debris – to assemble lipid nanodomains on cell surfaces of maturing cDCs, enhance expression of maturation markers, and stabilize immune receptor signaling. This process is dependent on cholesterol transport through Niemann-Pick disease type C1 (NPC1) and mediates homeostatic and TLR-induced maturation. Importantly, we identified the receptor tyrosine kinase AXL as a regulator of the NPC1-dependent construction of lipid nanodomains. Deleting AXL from cDCs enhances their maturation, thus improving antitumor immunity. Altogether, our study presents novel insights into cholesterol mobilization as a fundamental basis for cDC maturation and highlights AXL as a therapeutic target for modulating cDCs.

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Project description:Depending on how an antigen is perceived, dendritic cells (DCs) mature in an immunogenic or tolerogenic manner, safeguarding the balance between immunity and tolerance. Whereas the pathways driving immunogenic maturation in response to infectious insults are well characterized, the signals driving tolerogenic maturation in homeostasis are still poorly understood. Here we demonstrate that engulfment of apoptotic cells triggers homeostatic maturation of conventional cDC1s in the spleen. This process can be modeled by engulfment of empty, non-adjuvanted lipid nanoparticles (LNPs), is marked by intracellular accumulation of cholesterol, and highly unique to type 1 DCs. Engulfment of apoptotic cells or cholesterol-rich LNPs leads to activation of the LXR pathway driving cellular cholesterol efflux and repression of immunogenic genes. In contrast, simultaneous engagement of TLR3 to mimic viral infection via administration of poly(I:C)-adjuvanted LNPs represses the LXR pathway, thus delaying cellular cholesterol efflux and inducing genes that promote T cell immunity. These data demonstrate how DCs exploit the conserved cellular cholesterol efflux pathway to regulate induction of tolerance or immunity and reveal that administration of non-adjuvanted cholesterol-rich LNPs is a powerful platform for inducing tolerogenic DC maturation.

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