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RNA-Seq analysis of Tcf7-deficient and -sufficient lung CD8+ TRM cells after influenza infection

ABSTRACT: RNA-Seq analysis of Tcf7-deficient and -sufficient lung CD8+ TRM cells after influenza infection

PROVIDER: PRJNA558369 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9892972.fastq.gz	Fastqsanger.gz
	SRR9892973.fastq.gz	Fastqsanger.gz
	SRR9892974.fastq.gz	Fastqsanger.gz
	SRR9892975.fastq.gz	Fastqsanger.gz
	SRR9892976.fastq.gz	Fastqsanger.gz

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RNA-Seq analysis of Tcf7-deficient and -sufficient lung CD8+ TRM cells after influenza infection

Project description:T cell factor 1 (Tcf1, encoded by Tcf7) promotes the central memory CD8+ T cell (TCM) differentiation and homeostatic proliferation in lymphoid tissues. It remains unclear if and how Tcf1 regulates the CD103high tissue-resident memory CD8+ T cell (TRM) formation in non-lymphoid tissues. Using an influenza A infection mouse model, we collected Tcf7-deficient and -sufficient lung CD8+ TRM cells for RNA sequencing analysis.

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Project description:We set out to identify differences in the transcriptome influenced by knockout of the transcription factor T-cell factor 7 (Tcf7) in mouse islets. Furthermore, we wanted to determine if metabolic stress (age,diet) influences these changes. Therefore, we compared the islet transcriptome from WT and Tcf7-/- mice both at a young age (8 weeks old) fed a low fat (10%) diet, versus WT and Tcf7-/- mice at an old age (20 weeks old) on a high-fat (45%) diet. Tcf7-/- mice and littermate wildtype mice were compared. Mice were placed on either a low-fat (10%) or high-fat (45%) diet at weeks of age. For the low fat group, islets from 8 week old mice were isolated and total RNA was extracted with Trizol. For the high fat group, islets from 20 week old mice were isolated and total RNA was extracted with Trizol.

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ATAC sequencing of Tcf7 and Prdm1 deficient T cells [ATACseq_Tcf7Prdm1DKO]

Project description:The transcription factors Tcf7 (encoding TCF1) and Prdm1 (encoding Blimp1) exhibit opposing effects on T cell differentiation. While TCF1 promotes the maintenance of T progenitor exhausted cells, Blimp1 drives their differentiation into terminally exhausted effector cells. However, the impact of the combined deletion of these factors on CD8 T cell differentiation remains to be defined. We found that CD8 T cells in which TCF1 and Blimp1 are both ablated exhibit a TPEX surface phenotype in chronic infection but fail to expand in recall settings. To better understand how these factors poise T cells to respond to antigen encounter, bulk ATAC-sequencing was performed on TPEX cells from individual and combined transcription factor deficient CD8 T cells.

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