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

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

PROVIDER: PRJNA532724 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8893040.fastq.gz	Fastqsanger.gz
	SRR8893031.fastq.gz	Fastqsanger.gz
	SRR8893041.fastq.gz	Fastqsanger.gz
	SRR8893032.fastq.gz	Fastqsanger.gz
	SRR8893042.fastq.gz	Fastqsanger.gz

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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

Runx3-mediated transcriptional program in cytotoxic lymphocytes.

Project description:The transcription factor Runx3 is highly expressed in CD8(+) T and NK cytotoxic lymphocytes and is required for their effective activation and proliferation but molecular insights into the transcription program regulated by Runx3 in these cells are still missing. Using Runx3-ChIP-seq and transcriptome analysis of wild type vs. Runx3(-/-) primary cells we have now identified Runx3-regulated genes in the two cell types at both resting and IL-2-activated states. Runx3-bound genomic regions in both cell types were distantly located relative to gene transcription start sites and were enriched for RUNX and ETS motifs. Bound genomic regions significantly overlapped T-bet and p300-bound enhancer regions in Runx3-expressing Th1 helper cells. Compared to resting cells, IL-2-activated CD8(+) T and NK cells contain three times more Runx3-regulated genes that are common to both cell types. Functional annotation of shared CD8(+) T and NK Runx3-regulated genes revealed enrichment for immune-associated terms including lymphocyte activation, proliferation, cytotoxicity, migration and cytokine production, highlighting the role of Runx3 in CD8(+) T and NK activated cells.

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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.

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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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