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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.

2023-10-16 | PXD034920 | Pride

Transcriptome analysis of MAZR and/or Runx3-deficient cytotoxic T lymphocytes

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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CMV-specific cytotoxic T lymphocytes (CTLs) RNA-seq at the late phase of allo-HCT

Project description:CMV-specific cytotoxic T lymphocytes (CTLs) RNA-seq at the late phase of allo-HCT

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CMV-specific cytotoxic T lymphocytes (CTLs) RNA-seq at the early phase of allo-HCT

Project description:CMV-specific cytotoxic T lymphocytes (CTLs) RNA-seq at the early phase of allo-HCT

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RNA-seq of murine cytotoxic T lymphocytes unstimulated and stimulated with anti-CD3 for 10, 20, 40 and 60 minutes

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.

2023-10-15 | E-MTAB-12083 | biostudies-arrayexpress

A microRNA-directed program of cytotoxic CD8+ T cell differentiation

Project description:Acquisition of effector properties is a key step in the generation of cytotoxic T lymphocytes (CTLs). Here we show that inflammatory signals regulate Dicer expression in CTL, and that deletion or depletion of Dicer in mouse or human activated CD8+ T cells causes upregulation of perforin, granzyme and effector cytokines. Genome-wide analysis of miRNA changes induced by exposure of differentiating CTLs to IL-2 and inflammatory signals identifies miR-139 and miR-150 as components of a miRNA network that controls perforin, eomesodermin (Eomes) and IL-2Ra expression in differentiating CTLs and whose activity is modulated by IL-2, inflammation and antigenic stimulation. Overall our data show that strong IL-2R and inflammatory signals act through Dicer and miRNAs to control the cytolytic program and other aspects of effector CTL differentiation. Comparison of control and Dicer knock-out CTLs differentiated in vitro; Comparison of wild type CTLs differentiated in vitro with or without inflammatory stimuli; Comparison of effector and memory precursor CTLs isolated from mice infected with LCMV-Armstrong

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Project description:Celiac disease is an intestinal inflammatory disorder induced by dietary gluten in genetically susceptible individuals. The mechanisms underlying the massive expansion of interferon g–producing intraepithelial cytotoxic T lymphocytes (CTLs) and the destruction of the epithelial cells lining the small intestine of celiac patients have remained elusive. We report massive oligoclonal expansions of intraepithelial CTLs that exhibit a profound genetic reprogramming of natural killer (NK) functions. These CTLs aberrantly expressed cytolytic NK lineage receptors, such as NKG2C, NKp44, and NKp46, which associate with adaptor molecules bearing immunoreceptor tyrosine-based activation motifs and induce ZAP-70 phosphorylation, cytokine secretion, and proliferation independently of T cell receptor signaling. This NK transformation of CTLs may underlie both the self-perpetuating, gluten-independent tissue damage and the uncontrolled CTL expansion leading to malignant lymphomas in severe forms of celiac disease. Because similar changes were detected in a subset of CTLs from cytomegalovirus-seropositive patients, we suggest that a stepwise transformation of CTLs into NK-like cells may underlie immunopathology in various chronic infectious and inflammatory diseases. Keywords: NKG2C; LAK; CTL; NK receptor; IEL; Mucosal Immunity; Celiac Disease

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Dynamic and distinct transcriptional response of CD8+ cytotoxic T lymphocytes to tissue alarmins and adaptive cytokines

Project description:The respective effects of tissue alarmins like interleukin (IL)-15 and interferon beta (IFNb), and cytokines like IL-21 on the intraepithelial cytotoxic T lymphocytes (IE-CTLs) that cause autoimmune-mediated tissue destruction, is poorly understood. Analysis of the dynamics of transcriptomic and epigenomic profiles in primary IE-CTLs showed massive and distinct temporal transcriptional changes upon induction by tissue alarmins IL-15 and IFNb, while the impact of IL-21 was limited. Only anti-viral pathways were induced in response to all the three stimuli. Interestingly, the dynamically differentially expressed genes (DEGs), in particular genes in involved in IFN pathways, are enriched in autoimmune diseases risk loci. Changes in gene expression were primarily independent of changes in H3K27ac, but were enriched in differentially expressed non-coding (nc) RNAs. Together these results provide new insights into molecular mechanisms that fuel the activation of tissue resident CTLs under conditions that mimic aspects of the inflammatory environment in patients with immune-mediated diseases

2020-02-27 | GSE126409 | GEO

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