Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Oncolytic virus therapy mobilizes tumor-resident CD4+ bystander T cells to restore systemic anti-microbial immunity [ATAC-seq]

ABSTRACT: ATAC-seq library was prepared using Hyperactive ATAC-seq Library Prep Kit for Illumina (Vazyme, TD711) to study SM CD4+ T cells in lung and spleen when undergoing OV-BYTE treatment. Here, we further demonstrate that OV-BYTE delivered dual defense against tumorigenesis and pathogen infections in pre-clinical models. This study gives a epigenetic profiles of SM CD4+ T cells in lung and spleen with administration of OV-BYTE treatment.

ORGANISM(S): Mus musculus

PROVIDER: GSE302620 | GEO | 2025/08/06

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Oncolytic virus therapy mobilizes tumor-resident CD4+ bystander T cells to restore systemic anti-microbial immunity

Project description:The library preparation for single-cell RNA sequencing (scRNA-seq) using the BD Rhapsody platform to study SM CD4+ T cells in lung and spleen when undergoing OV-BYTE treatment. Here, we further demonstrate that OV-BYTE delivered dual defense against tumorigenesis and pathogen infections in pre-clinical models. This study gives a transcriptome profiles of SM CD4+ T cells in lung and spleen with administration of OV-BYTE treatment.

2025-08-06 | GSE302621 | GEO

Oncolytic virus therapy mobilizes tumor-resident CD4+ bystander T cells to restore systemic anti-microbial immunity [ATAC-seq]

Project description:Oncolytic virus therapy mobilizes tumor-resident CD4+ bystander T cells to restore systemic anti-microbial immunity [ATAC-seq]

| PRJNA1291592 | ENA

Oncolytic virus therapy mobilizes tumor-resident CD4+ bystander T cells to restore systemic anti-microbial immunity

Project description:Oncolytic virus therapy mobilizes tumor-resident CD4+ bystander T cells to restore systemic anti-microbial immunity

| PRJNA1291593 | ENA

Transcriptional profiling of Regulatory T cells isolated from mice exposed to Smoke, Morphine and Smoke plus Morphine

Project description:Purpose: The goals of this study were to identify gene expression signatures that are unique to Tregs from mice upon treatments with smoke, morphine and smoke plus morphine Methods and results: Wild-type mice were treated with cigarette smoke (SM) for a period of eight weeks, and/or the chronic continuous administration of morphine (M) via mini-pumps for the final four weeks CD4+CD25highCD127low Tregs from spleen were purified by cell sorting to generate mRNA transcription. Transcriptional profiling revealed a unique Treg signatures in SM, M or SM + M relative to control mice. Conclusion: Our study represents the first detailed analysis of splenic Treg transcriptome in mice exposure to smoke plus morphine.

2022-04-14 | GSE198210 | GEO

Vaccination Expands Antigen-Specific CD4+ Memory T Cells and Mobilizes Bystander Central Memory T Cells.

Project description:CD4+ T helper memory (Thmem) cells influence both natural and vaccine-boosted immunity, but mechanisms for their maintenance remain unclear. Pro-survival signals from the common gamma-chain cytokines, in particular IL-7, appear important. Previously we showed in healthy volunteers that a booster vaccination with tetanus toxoid (TT) expanded peripheral blood TT-specific Thmem cells as expected, but was accompanied by parallel increase of Thmem cells specific for two unrelated and non cross-reactive common recall antigens. Here, in a new cohort of healthy human subjects, we compare blood vaccine-specific and bystander Thmem cells in terms of differentiation stage, function, activation and proliferative status. Both responses peaked 1 week post-vaccination. Vaccine-specific cytokine-producing Thmem cells were predominantly effector memory, whereas bystander cells were mainly of central memory phenotype. Importantly, TT-specific Thmem cells were activated (CD38High HLA-DR+), cycling or recently divided (Ki-67+), and apparently vulnerable to death (IL-7RαLow and Bcl-2 Low). In contrast, bystander Thmem cells were resting (CD38Low HLA-DR- Ki-67-) with high expression of IL-7Rα and Bcl-2. These findings allow a clear distinction between vaccine-specific and bystander Thmem cells, suggesting the latter do not derive from recent proliferation but from cells mobilized from as yet undefined reservoirs. Furthermore, they reveal the interdependent dynamics of specific and bystander T-cell responses which will inform assessments of responses to vaccines.

| S-EPMC4557947 | biostudies-literature

ATAC-seq analysis in KPC1199 murine PDAC cell line with or without glutamine starvation

Project description:We determined if up- and/or down-regulated genes in pancreatic tumor cells cultured under low-glutamine conditions were accompanied by alterations in genome-wide chromatin accessibility and then performed ATAC-seq of KPC1199 cells treated with low glutamine concentrations versus normal-media-treated controls. The ATAC-seq was performed according to the TruePrep Tagment Enzyme for ATACseq kit (TD501, Vazyme). DNA libraries were constructed following the manufacturer’s instructions of the Trueprep index kit v2 (TD202, Vazyme) and thereafter sequenced to an average of 20 million reads per sample.

2024-04-30 | GSE229051 | GEO

Prmt5 deficiency inhibits CD4+T cells migration through Klf2-S1pr1 and ameliorates EAE disease (scRNA-seq)

Project description:Protein arginine methyltransferase 5 (Prmt5) is the major type II methyltransferase catalyzing symmetric dimethylation, regulates cell development, homeostatic and disease processes. Prmt5 inhibition or deletion in CD4+T cells has been reported to protection against experimental autoimmune encephalomyelitis (EAE), the perfect mouse model for multiple sclerosis (MS); however, the detail mechanisms have not yet been elucidated. Here, using the mRNA sequencing, single cell RNA sequencing and ATAC sequencing, we uncovered the unreported role of Prmt5 on T cells migration ability under the EAE condition. We found that mice condition knockout of Prmt5 in T cells were resistance with EAE, infiltrating inflammatory CD4+ T cells in center nervous system (CNS) were greatly reduced. However, T cells in spleen showed much more proliferation and activation properties in Prmt5cko mice, the number of pathogenic CD4+T cells in spleen were not reduced. We further revealed that Rora+CD4+T cells were elevated in Prmt5cko mice, but expressed lower level of S1pr1, resulting in a lack of CD4+ T cells egress from spleen and migrate to CNS, leading to pathogenic CD4+T cells were blocked in spleen. Moreover, single cell ATAC sequencing revealed that Klf2 were enriched in S1pr1 promoter and reduced in Prmt5cko mice. Correctively, our study delineated the undiscovered role of Prmt5 on T cell biology, Prmt5 may through Klf2-S1pr1 pathway and regulate T cells migration; modulating Prmt5 levels may be useful for controlling CD4+T cell migration in CD4+T cell mediated diseases including MS.

2023-08-09 | GSE195887 | GEO

Prmt5 deficiency inhibits CD4+T cells migration through Klf2-S1pr1 and ameliorates EAE disease (scATAC-seq)

2023-08-09 | GSE195882 | GEO

Prmt5 deficiency inhibits CD4+T cells migration through Klf2-S1pr1 and ameliorates EAE disease (RNA-seq)

2023-08-09 | GSE195874 | GEO

CUT&Tag analysis of H3K4me3 and Paxip1 in CRISPR/Cas9-mediated Paxip1 knockout KPC1199 murine PDAC cell line

Project description:To gain mechanistic insight into how Epigenetic factors reprogramming metabolism in response to DON treatment. we performed CUT&Tag sequencing in murine PDAC cells. sgPaxip1 cells were treated in Cont group or DON group , and harvested after 72 hours. CUT&Tag assay was performed following the manual of hyperactive pG-Tn5/pA-Tn5 transposase for CUT&Tag kit (TD901, Vazyme). DNA library were prepared according to manufacturer’s instructions of Trueprep index kit v2 (TD202, Vazyme).

2025-03-05 | GSE246545 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data