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Bcl6 mediates CD8+ T cell fate decision in cancer

ABSTRACT: Bcl6 mediates CD8+ T cell fate decision in cancer

PROVIDER: PRJNA754285 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15440761.fastq.gz	Fastqsanger.gz
	SRR15440762.fastq.gz	Fastqsanger.gz
	SRR15440763_1.fastq.gz	Fastqsanger.gz
	SRR15440763_2.fastq.gz	Fastqsanger.gz
	SRR15440764_1.fastq.gz	Fastqsanger.gz

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Project description:Overcoming CD8+ T cell "exhaustion" is critical in cancer immunotherapy. Intra-tumor CD8+ T cells contain stem-like (Texprog) and terminally differentiated (Texterm) subpopulations that mediate the persistence and potency of anti-tumor responses, respectively. How extrinsic signals via transcription factors control these two subsets are unclear. Previously, Bcl6 was shown to be selectively expressed by Texprog cells and promote their generation in chronic infection. Here, we found that in cancer, Bcl6 deficiency impacted, not the generation, but rather the persistence of Texprog cells, thus abrogating long-term tumor control. Bcl6 expression in CD8+ T cells is reciprocally regulated by TGF-?-SMAD2 and IL-2-STAT5 signaling pathways. Blimp1, regulated by IL-2 signaling, potently inhibited Bcl6 expression and its transcriptional activities; Prdm1 deficiency greatly improved the efficacy of anti-PD-1 therapy. Thus, we identified the TGF-?-Bcl6 and IL-2-Blimp1 antagonistic pathways in regulation of anti-tumor CD8+ T cells, which benefits cancer immunotherapy.

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Bcl6 mediates CD8+ T cell fate decision in cancer

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In vivo CRISPR screening reveals nutrient signaling processes underpinning CD8+ T cell fate decisions [microarray_dataset1]

Project description:The role of nutrient signaling processes in the fate decision of CD8 is incompletely understood. By performing in vivo pooled CRISPR-Cas9 screening, we uncovered nutrient signaling processes underpinning the dynamics and heterogeneity of CD8 T cell fate decisions.

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BCL6 mediates Chemoresistance in Acute Myeloid Leukemia

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