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Early precursor T cells establish and propagate T cell exhaustion in chronic infection [RNA-seq]

ABSTRACT: Early precursor T cells establish and propagate T cell exhaustion in chronic infection [RNA-seq]

PROVIDER: PRJNA597977 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10799665_1.fastq.gz	Fastqsanger.gz
	SRR10799665_2.fastq.gz	Fastqsanger.gz
	SRR10799666_1.fastq.gz	Fastqsanger.gz
	SRR10799666_2.fastq.gz	Fastqsanger.gz
	SRR10799667_1.fastq.gz	Fastqsanger.gz

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Early precursor T cells establish and propagate T cell exhaustion in chronic infection

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Early precursor T cells establish and propagate T cell exhaustion in chronic infection [ATAC-seq]

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Early precursor T cells establish and propagate T cell exhaustion in chronic infection [RNA-seq]

Project description:TCF1+ precursors of exhausted T cells maintain T cell immunity during chronic infection and cancer and mediate the response to immune checkpoint inhibition; however, their developmental requirements are poorly understood. Here, we demonstrate that high antigen load promoted the differentiation of TCF1+ precursor T cells, which acquired hallmarks of T cell exhaustion such as impaired production of IFN within the first days after infection. Transcriptional profiling revealed that exhaustion was established first in precursor T cells while early effector cells retained a polyfunctional profile. Early precursor T cells exposed to high amounts of antigen showed epigenetic imprinting of T cell receptor-dependent transcription factor binding, were dependent on BACH2 and restricted to the generation of T cells displaying features of exhaustion. Overall, we demonstrate that T cell exhaustion manifests first in TCF1+ precursor T cells and is propagated subsequently to the pool of antigen-specific T cells.

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Early precursor T cells establish and propagate T cell exhaustion in chronic infection [ATAC-seq]

Project description:TCF1+ precursors of exhausted T cells maintain T cell immunity during chronic infection and cancer and mediate the response to immune checkpoint inhibition; however, their developmental requirements are poorly understood. Here, we demonstrate that high antigen load promoted the differentiation of TCF1+ precursor T cells, which acquired hallmarks of T cell exhaustion such as impaired production of IFN? within the first days after infection. Transcriptional profiling revealed that exhaustion was established first in precursor T cells while early effector cells retained a polyfunctional profile. Early precursor T cells exposed to high amounts of antigen showed epigenetic imprinting of T cell receptor-dependent transcription factor binding, were dependent on BACH2 and restricted to the generation of T cells displaying features of exhaustion. Overall, we demonstrate that T cell exhaustion manifests first in TCF1+ precursor T cells and is propagated subsequently to the pool of antigen-specific T cells.

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Early precursor T cells establish and propagate T cell exhaustion in chronic infection

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2020-06-23 | GSE142687 | GEO

NFAT5 induction by the tumor microenvironment enforces CD8 T cell exhaustion [ATAC]

Project description:Persistent exposure to antigen during chronic infection or cancer renders T cells dysfunctional. The molecular mechanisms regulating this state of exhaustion are thought to be common in infection and cancer, despite obvious differences in their microenvironments. We discovered that NFAT5, an NFAT family member lacking an AP-1 docking site, is highly expressed in exhausted T cells responding to chronic infection and tumors but is a central player selectively in tumor-induced exhaustion. While NFAT5 overexpression in CD8+ T cells reduced tumor control, NFAT5 deletion improved tumor control by promoting the accumulation of tumor-specific CD8 T cells that expressed less TOX and PD-1 and produced more cytokines specifically among precursor exhausted cells. Conversely, NFAT5 did not promote T cell exhaustion during chronic infection. While NFAT5 expression was induced by TCR triggering, its transcriptional activity was specific to the tumor microenvironment and required hyperosmolarity. NFAT5 thus promotes CD8 T cell exhaustion in a tumor-selective fashion.

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NFAT5 induction by the tumor microenvironment enforces CD8 T cell exhaustion (CUT&Tag)

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Neonatal CD8+ T cells resist terminal exhaustion during chronic infection

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Neonatal CD8+ T cells resist terminal exhaustion during chronic infection [RNAseq_day30]

Project description:Neonatal CD8+ T cells resist terminal exhaustion during chronic infection [RNAseq_day30]

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Neonatal CD8+ T cells resist terminal exhaustion during chronic infection [RNAseq_day8]

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