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PD-L2 of tumor-derived exosomes mediates the immune escape of cancer cells via the impaired T cell function

ABSTRACT: PD-L2 of tumor-derived exosomes mediates the immune escape of cancer cells via the impaired T cell function

PROVIDER: PRJNA1014764 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25994008_1.fastq.gz	Fastqsanger.gz
	SRR25994008_2.fastq.gz	Fastqsanger.gz
	SRR25994009_1.fastq.gz	Fastqsanger.gz
	SRR25994009_2.fastq.gz	Fastqsanger.gz
	SRR25994010_1.fastq.gz	Fastqsanger.gz

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PD-L2 of tumor-derived exosomes mediates the immune escape of cancer cells via the impaired T cell function

Project description:The function and regulation of PD-1/PD-L1 axis have been widely studied for immune escape of various cancer cells. However, the underlying function and regulation of PD-L2 remain poorly to be understood. We demonstrate that PD-L2 is majorly secreted and expressed on exosomes with surface localization by tumor cell. In order to investigate the function of TDE-PD-L2 in the regulation of lymphocytes, we explored the expression profiles of TDE-PD-L2 on lymphocytes of PBMC using RNA-seq.

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Project description:In chronic lymphocytic leukemia (CLL), monocytes and macrophages are skewed toward protumorigenic phenotypes, including the release of tumor-supportive cytokines and the expression of immunosuppressive molecules such as programmed cell death 1 ligand 1 (PD-L1). To understand the mechanism driving protumorigenic skewing in CLL, we evaluated the role of tumor cell–derived exosomes in the cross-talk with monocytes. We carried out RNA sequencing and proteome analyses of CLL-derived exosomes and identified noncoding Y RNA hY4 as a highly abundant RNA species that is enriched in exosomes from plasma of CLL patients compared with healthy donor samples. Transfer of CLL-derived exosomes or hY4 alone to monocytes resulted in key CLL-associated phenotypes, including the release of cytokines, such as C-C motif chemokine ligand 2 (CCL2), CCL4, and interleukin-6, and the expression of PD-L1. These responses were abolished in Toll-like receptor 7 (TLR7)–deficient monocytes, suggesting exosomal hY4 as a driver of TLR7 signaling. Pharmacologic inhibition of endosomal TLR signaling resulted in a substantially reduced activation of monocytes in vitro and attenuated CLL development in vivo. Our results indicate that exosome-mediated transfer of noncoding RNAs to monocytes contributes to cancer-related inflammation and concurrent immune escape via PD-L1 expression.

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Impaired efferocytosis enables apoptotic osteoblasts to escape osteoimmune surveillance during aging (mRNA)

Project description:Impaired efferocytosis enables apoptotic osteoblasts to escape osteoimmune surveillance during aging (mRNA)

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Impaired efferocytosis enables apoptotic osteoblasts to escape osteoimmune surveillance during aging (mRNA)

Project description:Impaired efferocytosis enables apoptotic osteoblasts to escape osteoimmune surveillance during aging (mRNA)

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