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Tumor-Induced Erythroid Precursor-Differentiated Myeloid Cells Mediate Immunosuppression and Curtail Anti-PD-1/PD-L1 Treatment Efficacy

ABSTRACT: Tumor-Induced Erythroid Precursor-Differentiated Myeloid Cells Mediate Immunosuppression and Curtail Anti-PD-1/PD-L1 Treatment Efficacy

PROVIDER: PRJNA832746 | ENA |

REPOSITORIES: ENA

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			Action	DRS
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	SRR18944320_1.fastq.gz	Fastqsanger.gz
	SRR18944320_2.fastq.gz	Fastqsanger.gz
	SRR18944321_1.fastq.gz	Fastqsanger.gz
	SRR18944321_2.fastq.gz	Fastqsanger.gz

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Tumor-Induced Erythroid Precursor-Differentiated Myeloid Cells Mediate Immunosuppression and Curtail Anti-PD-1/PD-L1 Treatment Efficacy

Project description:Despite the unprecedented success of immune checkpoint inhibitors (ICIs) as anti-cancer therapy, it remains a prevailing clinical need to identify additional mechanisms underlying ICI therapeutic efficacy and potential drug resistance. Here, using lineage tracking in cancer patients and tumor-bearing mice, we demonstrate that erythroid progenitor cells lose their developmental potential and switch to the myeloid lineage. Single-cell transcriptome analyses reveal that, notwithstanding quantitative differences in erythroid gene expression, erythroid differentiated myeloid cells (EDMCs) are transcriptionally indistinguishable from their myeloid-originated counterparts. EDMCs possess multifaceted machinery to curtail T cell-mediated anti-tumor responses. Consequently, EDMC content within tumor tissues is negatively associated with T cell inflammation for the majority of solid cancers; moreover, EDMC enrichment, in accordance with anemia manifestation, is predictive of poor prognosis in various cohorts of patients undergoing ICI therapy. Together, our findings reveal a feed-forward mechanism by which tumors exploit anemia-triggered erythropoiesis for myeloid transdifferentiation and immunosuppression.

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