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MRNA-seq analysis of mouse cytotoxic T lymphocytes (CTLs) over-expressing Akt isoforms

ABSTRACT: mRNA-seq analysis of mouse cytotoxic T lymphocytes (CTLs) over-expressing Akt isoforms

PROVIDER: PRJNA634844 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11840704_1.fastq.gz	Fastqsanger.gz
	SRR11840704_2.fastq.gz	Fastqsanger.gz
	SRR11840705_1.fastq.gz	Fastqsanger.gz
	SRR11840705_2.fastq.gz	Fastqsanger.gz
	SRR11840706_1.fastq.gz	Fastqsanger.gz

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mRNA-seq analysis of mouse cytotoxic T lymphocytes (CTLs) over-expressing Akt isoforms

Project description:PI3K/Akt pathway plays a central role in T-cell activation and is impaired in Ag-specific CTLs during chronic viral infections. In this study, we genetically engineered HBV-specific CTLs and adoptively transferred these Akt-expressing viral Ag-specific CTLs into HBV-infected mice and monitored the virological and immunological responses. In the meantime, we also analyzed the mRNA profiles of control-CTLs and CTLs-overexpressing Akt1 and Akt2, respectively before adoptive transfer and after in vitro restimulation. We expect to elucidate the potential mechanisms about how the Akt signaling in CTLs prevents T-cell exhaustion and enhance T-cell expansion in the liver during persistent HBV infection from this mRNA-seq analysis.

2025-01-03 | GSE151131 | GEO

Actinomycin D treated cytotoxic T lymphocytes

Project description:Effector cytotoxic T lymphocytes (CTLs) are critical for ridding the body of infected or cancerous cells. Recognition of an antigenic ligand by the CTL’s T cell receptor (TCR) triggers a signalling cascade that ultimately results in the targeted release of cytolytic granules and/or secretion of cytokines and chemokines to alert and recruit additional immune cells. These signalling cascades are capable of initiating transcription, translation, and cytoskeletal rearrangements. While previous work has demonstrated how translation and intracellular reorganisation contribute to CTL effector responses, the role of transcription is less well studied. To address this, we examined the impact of blocking transcription on the CTL proteome during TCR stimulation. These data demonstrated a strong transcriptional requirement for expression of cytokines and chemokines but not cytolytic molecules. Together with functional studies, these data reveal differential molecular control of the cell-cell communication and cytolytic functions of effector CTLs. CTLs exhibit complete and persistent priming for cytolytic activity prior to target cell encounter, but they require de novo transcription to recruit additional immune cells that amplify the response.

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Project description:We investigated transcriptional changes in MAZR-, Runx3- and MAZR/Runx3-deficient cytotoxic T lymphocytes (CTLs). This analysis revealed that MAZR plays a compensatory role in the Runx3-dependent transcriptional program of CTL differentiation.

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Project description:We wished to examine early transcriptional changes that occur after TCR engagement in CD8+ cytotoxic T lymphocytes (CTLs). To this end, we differentiated effector CTLs from OTI TCR transgenic mice for 7 days in vitro and then stimulated them with anti-CD3 for various times before lysing for RNA-seq. Results demonstrated significant transcriptional changes starting from 20 minutes. After 60 minutes, upregulated genes were most enriched for cytokines and transcriptional machinery.

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Expression data from control and Phospholipid dependent kinase 1 (PDK1) null cytotoxic T-lymphocytes (CTL) and from control and Akt inhibitor treated CTL

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Super-killer CTLs are generated by single gene deletion of Bach2

Project description:Bach2 codes for a transcriptional regulator exerting major influences on T cell mediated immune regulation. Effector CTLs derived from in vitro activation of murine CD8+ T cells showed increased proliferative and cytolytic capacity in the absence of BACH2. Before activation, BACH2-deficient CD8+ T cells had a higher abundance of memory and reduced abundance of naïve cells compared to wild-type. CTLs derived from central memory T cells were more potently cytotoxic than those derived from naïve T cells, but even within separated subsets, BACH2-deficiency conferred a cytotoxic advantage. Immunofluorescence and electron microscopy revealed larger granules in BACH2-deficient compared to wild-type CTLs, and proteomic analysis showed an increase in granule content, including perforin and granzymes. Thus, the enhanced cytotoxicity observed in effector CTLs lacking BACH2 arises not only from differences in their initial differentiation state but also inherent production of enlarged cytolytic granules. These results demonstrate how a single gene deletion can produce a CTL super-killer.

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Expression data from control and Phospholipid dependent kinase 1 (PDK1) null cytotoxic T-lymphocytes (CTL) and from control and Akt inhibitor treated CTL

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