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Autophagy Suppresses CD8+ T cell Anti-tumour Immunity

ABSTRACT: Autophagy Suppresses CD8+ T cell Anti-tumour Immunity

PROVIDER: PRJNA483127 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7609953_1.fastq.gz	Fastqsanger.gz
	SRR7609953_2.fastq.gz	Fastqsanger.gz
	SRR7609954_1.fastq.gz	Fastqsanger.gz
	SRR7609954_2.fastq.gz	Fastqsanger.gz
	SRR7609955_1.fastq.gz	Fastqsanger.gz

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Autophagy Suppresses CD8+ T cell Anti-tumour Immunity

Project description:Here we demonstrate that inactivation of the essential autophagy genes, Atg5, Atg14, or Atg16L1 results in tumour rejection. Despite a significant reduction in the total number of CD8+ tumour infiltrating lymphocytes (TILs), loss of Atg5 causes a profound shift toward IFNg and TNF producing effector memory cells. Consistent with this, adoptive transfer with Atg5-/- T cells promotes tumour control. Mechanistically, CD8+ T cells lacking autophagy exhibit enhanced glucose metabolism resulting in global changes in histone trimethylation and increased transcriptional activation of effector target genes. Restricting glucose is sufficient to suppress autophagy-dependent increases in effector function and reverse alterations in histone trimethylation. These findings identify autophagy as a cell-autonomous negative regulator of CD8+ T cell anti-tumour immunity with implications on T cell-based immunotherapy.

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Spatial organization of tumour cDC1 states correlates with effector and stem-like CD8+ T cells location

Project description:CD8+ T cells are central to targeting and eliminating cancer cells. Their function is critically supported by type 1 conventional dendritic cells (cDC1s), which both prime antigen-specific CD8+ T cells in tumour-draining lymph nodes (tdLNs) and sustain primed CD8+ T cells within tumours. Despite their importance, the spatiotemporal organisation of cDC1s within tumours and their diverse functional roles remain poorly understood. Here, we use scRNAseq and unbiased spatial analysis to construct a detailed map of cDC1 states and distribution within immunogenic mouse tumours during CD8+ T cell-mediated rejection. We reveal two distinct cDC1 activation states characterised by differential expression of genes linked to anti-tumour immunity, including Cxcl9 and Il12b. Strikingly, Il12b-expressing cDC1s are CCR7+ and enriched at tumour borders, where they closely associate with stem-like TCF1+ CD8+ T cells. In contrast, CCR7– Cxcl9-expressing cDC1s are preferentially found within the tumour parenchyma alongside effector CD8+ T cells. Analysis of a published dataset of human tumours similarly reveals a spatial association between CCR7+ cDC1 and stem-like TCF1+ CD8+ T cells. These findings uncover a highly spatially coordinated interaction between cDC1s and CD8+ T cells within tumours, shedding light on the intricate cellular dynamics that underpin effective anti-tumour immunity.

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Tumor-intrinsic expression of the autophagy gene Atg16l1 suppresses anti-tumor immunity in colorectal cancer

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