RNA-seq of tumor residing CD8+ T cells overexpressing Runx3
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA419738 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6321774_1.fastq.gz | Fastqsanger.gz | |||
| SRR6321774_2.fastq.gz | Fastqsanger.gz | |||
| SRR6321775_1.fastq.gz | Fastqsanger.gz | |||
| SRR6321775_2.fastq.gz | Fastqsanger.gz | |||
| SRR6321776_1.fastq.gz | Fastqsanger.gz |
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Project description:Tissue-resident memory CD8+ T cells (Trm) are positioned at common sites of pathogen exposure where they elicit rapid and robust protective immune responses1,2. However, the molecular signals controlling Trm differentiation and homeostasis are not fully understood. Here we show that mouse Trm precursor cells represent a unique CD8+ T cell subset that is distinct from the precursors of circulating memory populations at the levels of gene expression and chromatin accessibility. Exploiting computational and functional RNAi in vivo screens, we identified the transcription factor (TF) Runx3 as a key regulator of Trm differentiation and homeostasis. Runx3 was required to establish Trm populations in diverse tissue environments and supported expression of critical tissue-residency genes while suppressing genes associated with tissue egress and recirculation. Analysis of the accessibility of Runx3 target genes in Trm-precursor cells revealed a distinct regulatory role for Runx3 in controlling Trm differentiation despite relatively widespread and uniform expression among all CD8+ T cell subsets. Further, we show that human and murine tumor-infiltrating lymphocytes (TIL) share a core tissue-residency gene-expression signature with Trm. In a mouse model of adoptive T cell therapy for melanoma, Runx3-deficient CD8+ TIL failed to accumulate in tumors, resulting in greater rates of tumor growth and mortality. Conversely, overexpression of Runx3 enhanced TIL abundance, delayed tumor growth, and prolonged survival. In addition to establishing Runx3 as a central regulator of Trm differentiation, these results provide novel insight into the signals that promote T cell residency in tissues, which could be leveraged to enhance vaccine efficacy or adoptive cell therapy treatments that target cancer.
2017-12-15 | GSE107289 | GEO
Project description:CD8+T cells are immune cells that recognize foreign antigens on infected and tumor cells, leading to cytokine-dependent expansion and activation of cytotoxicity towards the targets. To identify Runx3 responsive genes, CD8+ T cells were isolated from spleen of WT and Runx3-/- mice . Six samples (3 WT and 3 Runx3-/-) of freshly isolated CD8+ T cells (resting) were separately obtained from individual mice.
2013-11-18 | E-GEOD-50119 | biostudies-arrayexpress
Project description:CD8+T cells are immune cells that recognize foreign antigens on infected and tumor cells, leading to cytokine-dependent expansion and activation of cytotoxicity towards the targets. To identify Runx3 regulated genes, CD8+ T cells were isolated from spleen of WT and Runx3-/- mice . Six samples (3 WT and 3 Runx3-/-) of CD8+ T cells were separately obtained from individual mice, TCR activated and cultured for 4 days with IL-2.
2013-11-18 | E-GEOD-50121 | biostudies-arrayexpress
Project description:ChIP-seq was conducted using freshly isolated (resting) splenic WT CD8+ T cells with anti-Runx3 antibody (Ab), anti-H3K4me1 Ab and non-immune serum (NIS) as control. Two biological Runx3 and two NIS IP repeats from splenic CD8+ T cells isolated by positive selection on anti-CD8 magnetic beads, collected from 18 WT mice.
2013-11-18 | E-GEOD-50130 | biostudies-arrayexpress
Project description:ChIP-seq was conducted on isolated splenic WT CD8+ T cells, TCR-activated and cultured with IL-2 using anti-Runx3 antibodies (Ab), anti-H3K4me1 Ab and non-immune serum (NIS) as control. Two biological Runx3 and two NIS IP repeats from TCR-activated and IL-2 cultured splenic CD8+ T cells isolated by positive selection on anti-CD8 magnetic beads.
2013-11-18 | E-GEOD-50128 | biostudies-arrayexpress
Project description:Runx3 is an important transcription factor for the proper development of CD8+T cells. The number and functionality of CD8+T cells is severely affected in the absence of Runx3. To gain insight into the transcriptional program managed by Runx3 in CD8+T cells we conducted ChIP-seq on 50 million cells and CUT&RUN on 150,000 cells, using anti Runx3 antibodies. Both assays revealed similar results.
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Project description:Cellular binary fate decisions require the progeny to silence genes associated with the alternative fate. The major subsets of alpha:beta T cells have been extensively studied as a model system for fate decisions. While the transcription factor RUNX3 is required for the initiation of Cd4 silencing in CD8 T cell progenitors, it is not required to maintain the silencing of Cd4 and other helper T lineage genes. The other runt domain containing protein, RUNX1, silences Cd4 in an earlier T cell progenitor, but this silencing is reversed whereas the gene silencing after RUNX3 expression is not reverse. Therefore, we hypothesized that RUNX3 and not RUNX1 recruits other factors that maintains the silencing of helper T lineage genes in CD8 T cells. To this end, we performed a proteomics screen of RUNX1 and RUNX3 to determine candidate silencing factors.
2019-11-12 | PXD007511 | Pride
Project description:Tissue-resident memory CD8+ T cells (Trm) are positioned at common sites of pathogen exposure where they elicit rapid and robust protective immune responses. However, the molecular signals controlling Trm differentiation and homeostasis are not fully understood. Here we show that mouse Trm precursor cells represent a unique CD8+ T cell subset that is distinct from the precursors of circulating memory populations at the levels of gene expression and chromatin accessibility. Exploiting computational and functional RNAi in vivo screens, we identified the transcription factor (TF) Runx3 as a key regulator of Trm differentiation and homeostasis. Runx3 was required to establish Trm populations in diverse tissue environments and supported expression of critical tissue-residency genes while suppressing genes associated with tissue egress and recirculation. Analysis of the accessibility of Runx3 target genes in Trm-precursor cells revealed a distinct regulatory role for Runx3 in controlling Trm differentiation despite relatively widespread and uniform expression among all CD8+ T cell subsets. Further, we show that human and murine tumor-infiltrating lymphocytes (TIL) share a core tissue-residency gene-expression signature with Trm. In a mouse model of adoptive T cell therapy for melanoma, Runx3-deficient CD8+ TIL failed to accumulate in tumors, resulting in greater rates of tumor growth and mortality. Conversely, overexpression of Runx3 enhanced TIL abundance, delayed tumor growth, and prolonged survival. In addition to establishing Runx3 as a central regulator of Trm differentiation, these results provide novel insight into the signals that promote T cell residency in tissues, which could be leveraged to enhance vaccine efficacy or adoptive cell therapy treatments that target cancer.
2018-01-03 | GSE106107 | GEO
Project description:Comparison of transcriptome between control and Runx3-deficient CD8 effector T cells
2017-05-16 | GSE81885 | GEO
Project description:Define how ablating Runx3 affects histone marks and active enhancers in early effector CD8 T cells
2017-05-16 | GSE81887 | GEO