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Bulk RNA-Seq profiling of progenitor exhausted (Slamf6+Tim-3-) and terminally exhausted (Slamf6-Tim-3+) CD8+ T-cells from tumors and chronic viral infection

ABSTRACT: Bulk RNA-Seq profiling of progenitor exhausted (Slamf6+Tim-3-) and terminally exhausted (Slamf6-Tim-3+) CD8+ T-cells from tumors and chronic viral infection

PROVIDER: PRJNA507854 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8269910_1.fastq.gz	Fastqsanger.gz
	SRR8269910_2.fastq.gz	Fastqsanger.gz
	SRR8269920_1.fastq.gz	Fastqsanger.gz
	SRR8269920_2.fastq.gz	Fastqsanger.gz
	SRR8269930_1.fastq.gz	Fastqsanger.gz

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Bulk RNA-Seq profiling of progenitor exhausted (Slamf6+Tim-3-) and terminally exhausted (Slamf6-Tim-3+) CD8+ T-cells from tumors and chronic viral infection

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Project description:Chronic antigen stimulation is thought to generate dysfunctional CD8 T cells. Here we identify a CD8 T cell subset in the bone marrow tumor microenvironment that, despite an apparent terminally exhausted phenotype (TPHEX), expressed granzymes, perforin, and IFNγ. Concurrent gene expression and DNA accessibility revealed that genes encoding these functional proteins correlated with BATF expression and motif accessibility. IFNγ+ TPHEX effectively killed myeloma with comparable efficacy to transitory effectors, and disease progression correlated with numerical deficits in IFNγ+ TPHEX. We also observed IFNγ+ TPHEX within CD19-targeted chimeric antigen receptor T cells, which killed CD19+ leukemia cells. Importantly, an IFNγ+ TPHEX gene signature was recapitulated in TEX cells from human cancers, including myeloma and lymphoma. Here we characterize a TEX subset in hematological malignancies that paradoxically retains function and is distinct from dysfunctional TEX found in chronic viral infections. Thus, IFNγ+ TPHEX represent a potential target for immunotherapy of blood cancers.

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