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Effect of SRSF1 splicing factor knockdown in the physiology and function of cytotoxic CD8 T lymphocytes and a potential molecular mechanism in viral immunopathogenesis

ABSTRACT: Effect of SRSF1 splicing factor knockdown in the physiology and function of cytotoxic CD8 T lymphocytes and a potential molecular mechanism in viral immunopathogenesis

PROVIDER: PRJNA828104 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18809823_1.fastq.gz	Fastqsanger.gz
	SRR18809823_2.fastq.gz	Fastqsanger.gz
	SRR18809824_1.fastq.gz	Fastqsanger.gz
	SRR18809824_2.fastq.gz	Fastqsanger.gz
	SRR18809825_1.fastq.gz	Fastqsanger.gz

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Effect of SRSF1 splicing factor knockdown in the physiology and function of cytotoxic CD8 T lymphocytes and a potential molecular mechanism in viral immunopathogenesis

Project description:Cytotoxic CD8 T cells are crucial for the host antigen-specific immune response to viral pathogens. Here we report the identification of an essential role for the serine/arginine-rich splicing factor (SRSF) 1 in CD8 T cell homeostasis and function Transcriptomics analyses of Srsf1-deficient T cells reveal that SRSF1 controls cell cycle, MAP kinase signaling and IFN signaling pathways.

2022-07-31 | GSE201028 | GEO

Loss of canonical splicing factor SRSF1 in hepatocytes results in acute liver injury and regeneration

Project description:Post-transcriptional gene regulatory mechanisms (PTGRM) contribute profoundly to liver development and physiology. Alternative splicing is one of the earliest mechanisms of gene regulation acting on nascently transcribed mRNA. This process is mediated by a large class of proteins known as splicing factors. SRSF1 is a canonical splicing factor with roles in both constitutive and alternative splicing. While its biochemical activities have been studied extensively, its role in tissue physiology are not well defined. In this study we investigate the role of SRSF1 in liver physiology using hepatocyte-specific knock-out mice models. Hepatocyte-specific knock-out of SRSF1 was achieved in two ways; 1) SRSF1 floxed mice were crossed with AlbCre transgenic mice and 2) SRSF1 floxed mice were injected with AAV8-TBG-iCre viral vector. The latter model allowed for investigating acute changes in hepatocyte upon ablation of SRSF1. Both models exhibit acute liver injury with severe cellular damage, inflammation and lipid accumulation. Utilizing high-throughput transcriptome profiling on purified hepatocytes, we find acute loss of SRSF1 triggers activation of the p53 pathway and splicing dysregulation of genes involved in mRNA metabolism. Continuous hepatic injury in this model eventually triggers a regenerative response resulting in the upregulation of genes involved in proliferation and repopulation of the tissue parenchyma.

2021-03-31 | GSE147005 | GEO

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.

2021-03-11 | GSE129772 | GEO

Personalized neoantigen-based T cell therapy triggers cytotoxic lymphocytes expressing polyclonal TCR against metastatic ovarian cancer

Project description:Neoantigen-reactive cytotoxic T lymphocytes play a vital role in precise cancer cell elimination. In this study, we demonstrate the effectiveness of personalized neoantigen-based T cell therapy in inducing tumor regression in two patients suffering from heavily-burdened metastatic ovarian cancer. Our approach involved the development of a robust pipeline for ex vivo expansion of neoantigen-reactive T lymphocytes. Neoantigen peptides were designed and synthesized based on the somatic mutations of the tumors and their predicted HLA binding affinities. These peptides were then presented to T lymphocytes through co-culture with neoantigen-loaded dendritic cells for ex vivo expansion. Subsequent to cell therapy, both patients exhibited significant reductions in tumor marker levels and experienced substantial tumor regression. One patient achieved repeated cancer regression through infusions of T cell products generated from newly identified neoantigens. Transcriptomic analyses revealed a remarkable increase in neoantigen-reactive cytotoxic lymphocytes in the peripheral blood of the patients following cell therapy. These cytotoxic T lymphocytes expressed polyclonal T cell receptors (TCR) against neoantigens, along with abundant cytotoxic proteins and pro-inflammatory cytokines. The efficacy of neoantigen targeting was significantly associated with the immunogenicity and TCR polyclonality. Notably, the neoantigen-specific TCR clonotypes persisted in the peripheral blood after cell therapy. Our findings indicate that personalized neoantigen-based T cell therapy triggers cytotoxic lymphocytes expressing polyclonal TCR against ovarian cancer, suggesting its promising potential in cancer immunotherapy.

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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:The mechanistic target of rapamycin (mTOR) signaling, which is an essential metabolic pathway that influences T cell differentiation, can be limited under conditions of metabolic stress e.g. during the cell starvation. As we observed reduced CD8 expression upon cell starvation in vitro, we sorted human cytotoxic T lymphocytes derived from six donors into low CD8 expression and high CD8 expressing T lymphocytes using flow cytometry. Their transcriptome was analyzed in order to investigate the two CD8 subsets. Our data suggests a functional diversity of CD8low and CD8high T cells with regard to cytotoxic effector function that might be useful to study these cells also in tumor sections or under conditions when cytotoxic T cells need to adapt to a changing microenvironment.

2022-09-30 | GSE207621 | GEO

In-depth analysis of the phosphoprotein landscape of cytotoxic T lymphocytes and its regulation by cytokines

Project description:Here we present high-resolution mass spectrometry analysis of changes to the phosphoproteome of cytotoxic T lymphocytes (CTL) induced by the cytokine, Interleukin 12 (IL-12). We treated CTL with a short and long IL-12 stimulation and mapped the changes to the phosphoproteome using quantitative SILAC-based phosphoproteomics.

2016-08-24 | PXD004644 | Pride

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

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