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Type I interferon activates MHC class I-dressed CD11b+ conventional dendritic cells to promote protective anti-tumor CD8+ T cell immunity

ABSTRACT: Type I interferon activates MHC class I-dressed CD11b+ conventional dendritic cells to promote protective anti-tumor CD8+ T cell immunity

PROVIDER: PRJNA753931 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15421244_1.fastq.gz	Fastqsanger.gz
	SRR15421244_2.fastq.gz	Fastqsanger.gz
	SRR15421245_1.fastq.gz	Fastqsanger.gz
	SRR15421245_2.fastq.gz	Fastqsanger.gz
	SRR15421246_1.fastq.gz	Fastqsanger.gz

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Type I interferon activates MHC class I-dressed CD11b+ conventional dendritic cells to promote protective anti-tumor CD8+ T cell immunity

Project description:Type I interferon activates MHC class I-dressed CD11b+ conventional dendritic cells to promote protective anti-tumor CD8+ T cell immunity

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Type I interferon activates MHC class I-dressed CD11b+ conventional dendritic cells to promote protective anti-tumor CD8+ T cell immunity

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Type I interferon activates MHC class I-dressed CD11b+ conventional dendritic cells to promote protective anti-tumor CD8+ T cell immunity

Project description:Tumor-infiltrating antigen-presenting cells, such as dendritic cells (DC), have the capacity to shape anti-tumor T cell responses. While tremendous progress has been made in unraveling the role of Batf3-driven DC1 in the anti-tumor immune response, the contributions of other tumor-infiltrating DC subsets remain poorly understood. Furthermore, tumor-infiltrating DC exist in a range of functional states with differential impacts on anti-tumor immunity. In this study, we sought to identify and characterize the functionally relevant DC states associated with a productive anti-tumor T cell response. By comparing the DC infiltrate of spontaneously regressing tumors and progressing tumors, we identified a novel activation state of CD11b+ conventional DC in tumors, which expressed an interferon-stimulated gene signature (‘ISG+ DC’). ISG+ DC were activated by type-I-interferon-induced signaling and could generate protective CD8+ T cell responses by cross-dressing with tumor-derived peptide-MHC complexes. Stimulatory ISG+ DC induced by exogenous IFNβ addition drove robust anti-tumor T cell responses in poorly immunogenic tumors even in the absence of DC1.

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