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Rebalancing TGFβ1/BMP Signals Preserves Effector and Memory Programs in Terminally Dysfunctional CD8+ T Cells [RNA-Seq]

ABSTRACT: Rebalancing TGFβ1/BMP Signals Preserves Effector and Memory Programs in Terminally Dysfunctional CD8+ T Cells [RNA-Seq]

PROVIDER: PRJNA896866 | ENA |

REPOSITORIES: ENA

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Rebalancing TGFβ1/BMP Signals Preserves Effector and Memory Programs in Terminally Dysfunctional CD8+ T Cells [Bisulfite-Seq]

Project description:T cell dysfunctionality prevents clearance of chronic infections and cancer. Furthermore, epigenetic programming in dysfunctional CD8+ T cells limits durable responses to T cell-based immunotherapies, including immune checkpoint blockade (ICB). However, major gaps concern how upstream signals drive acquisition of dysfunctional epigenetic programs, and whether therapeutically targeting these signals can remodel terminally dysfunctional T cells to an ICB-responsive state. Here, we use an in vitro model of human T cell dysfunction and complementary in vivo mouse chronic virus infection and tumor models. We show that post-effector TGFβ1 signaling establishes terminal dysfunction in human CD8+ T cells through stable epigenetic changes. Importantly, we demonstrate that promoting BMP signaling while blocking TGFβ1 restored effector and memory programs in dysfunctional human CD8+ T cells, induced superior anti-tumor activity, and boosted ICB responses during mouse chronic virus infection. Thus, rebalancing TGFβ1/BMP-signals in dysfunctional CD8+ T cells provides an exciting new approach to enhance T cell immunotherapies.

2022-11-03 | GSE217087 | GEO

Rebalancing TGFβ1/BMP Signals Preserves Effector and Memory Programs in Terminally Dysfunctional CD8+ T Cells [RNA-Seq]

2022-11-03 | GSE217072 | GEO

Rebalancing TGFβ1/BMP Signals Preserves Effector and Memory Programs in Terminally Dysfunctional CD8+ T Cells

Project description:Rebalancing TGFβ1/BMP Signals Preserves Effector and Memory Programs in Terminally Dysfunctional CD8+ T Cells

| PRJNA896918 | ENA

Rebalancing TGFβ1/BMP Signals Preserves Effector and Memory Programs in Terminally Dysfunctional CD8+ T Cells [Bisulfite-Seq]

Project description:Rebalancing TGFβ1/BMP Signals Preserves Effector and Memory Programs in Terminally Dysfunctional CD8+ T Cells [Bisulfite-Seq]

| PRJNA896920 | ENA

Rebalancing TGFβ1/BMP Signals Preserves Effector and Memory Programs in Terminally Dysfunctional CD8+ T Cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-11-03 | GSE217088 | GEO

TGFβ1 treatment of A2058 melanoma cells

Project description:4 replicates were prepared from A2058 melanoma cells [transfected with 10ng of empty vector (pcDNA3.1+)] and treated with 5ng/ml TGFβ1 or vehicle control for 24hrs This is the control arm of a larger experiment where cells transfected with a particular expression plasmid were treated with TGFβ1 or control vehicle. The transfection with the expresion plasmid was unsucessful so this empty vector data has been used alone to simply examine the effect of TGFβ1 treatment on A2058 cells.

2015-02-20 | E-GEOD-66114 | biostudies-arrayexpress

RNA-seq analysis of FET cells treated with RSPO1 or TGFβ1

Project description:To determine whether RSPO1 and TGFβ1 activate similar transcription, RNA-seq analysis was performed to compare gene profiles after treatment by RSPO1 or TGFβ1. FET cells were treated with RSPO1 or TGFβ1 in triplicates for 4 hours and RNAs extracted from these cells were used for RNA-seq analysis. When gene expression profiles were compared, it was found that 153 genes were commonly regulated by either RSPO1 or TGFβ1. Interestingly, the majority of genes regulated by TGFβ1 were also regulated by RSPO1.

2017-09-09 | GSE103650 | GEO

Development and Preclinical Efficacy of Novel Transforming Growth Factor-β1 (TGFβ1) siRNAs for Pulmonary Fibrosis

Project description:Idiopathic pulmonary fibrosis is a chronic devastating disease of unknown etiology. No therapy is currently available. A growing body of evidence supports the role of TGFβ1 as the major player in the pathogenesis of the disease. This study designed novel human- and mouse-specific siRNAs and siRNA/DNA chimeras targeting both human and mouse common sequences and evaluated their inhibitory activity in pulmonary fibrosis induced by bleomycin and lung-specific transgenic expression of human TGFβ1. Selective novel sequences of siRNA and siRNA/DNA chimeras efficiently inhibited pulmonary fibrosis, indicating their applicability as tools for treating fibrotic disease in humans. Total RNA was extracted from lung tissue from mice with bleomycin (BLM)-induced lung fibrosis treated with mouse TGFβ1 siRNAs or vehicle on different days after BLM infusion.

2011-11-22 | E-GEOD-28122 | biostudies-arrayexpress

TGFβ1 treatment of A2058 melanoma cells

Project description:4 replicates were prepared from A2058 melanoma cells [transfected with 10ng of empty vector (pcDNA3.1+)] and treated with 5ng/ml TGFβ1 or vehicle control for 24hrs

2015-02-20 | GSE66114 | GEO

GPCR-induced YAP activation sensitizes fibroblasts to profibrotic effects of TGFβ1

Project description:Fibrosis is an uncontrolled wound healing process resulting from tissue injury, inflammation and fibroblast activation, finally leading to accumulation of extracellular matrix (ECM) components in tissues and to organ failure. The underlying mechanisms of fibrosis have been intensely studied and it has become clear that multiple pathways and their crosstalk regulate fibrotic diseases with a few central players, including TGFβ1. Recently, YAP and TAZ were implicated in fibrosis as one of the essential components of its pathogenesis. YAP/TAZ are known to crosstalk with the TGFβ pathway in the nucleus and regulate its activity on transcriptional level by binding to Smad2/3/4 complexes. We hypothesized that factors, such as GPCR ligands which regulate YAP/TAZ, might modulate the profibrotic responses to TGFβ1. We performed gene expression microarray in NHDF treated with TGFβ1, LPA, the combination of TGFβ1/LPA or vehicle. The aim was to have a broader look at transcriptional signatures induced by the individual treatments and in the combination of TGFβ1 and LPA.

2020-01-27 | GSE125519 | GEO

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