Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

PD-1 is imprinted on cytomegalovirus-specific CD4+ T cells and attenuates Th1 cytokine production whilst maintaining cytotoxicity

ABSTRACT: PD-1 is imprinted on cytomegalovirus-specific CD4+ T cells and attenuates Th1 cytokine production whilst maintaining cytotoxicity

PROVIDER: PRJNA698638 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR13606105_1.fastq.gz	Fastqsanger.gz
	SRR13606105_2.fastq.gz	Fastqsanger.gz
	SRR13606106_1.fastq.gz	Fastqsanger.gz
	SRR13606106_2.fastq.gz	Fastqsanger.gz
	SRR13606107_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 26

Similar Datasets

PD-1 is imprinted on cytomegalovirus-specific CD4+ T cells and attenuates Th1 cytokine production whilst maintaining cytotoxicity

Project description:PD-1 is expressed on exhausted T cells in cancer patients but its physiological role remains uncertain. We determined the phenotype, function and transcriptional correlates of PD-1 expression on cytomegalovirus-specific CD4+ T cells during latent infection. PD-1 expression ranged from 10-85% and remained stable over time within individual donors. This ‘setpoint’ was correlated with viral load at primary infection. PD-1+ CD4+ T cells display strong cytotoxic function but generate low levels of Th1 cytokines which is only partially reversed by PD-1 blockade. TCR clonotypes showed variable sharing between PD-1+ and PD-1- CMV-specific cells indicating that PD-1 status is defined either during T cell priming or subsequent clonal expansion. Physiological PD-1+ CD4+ T cells therefore display a unique ‘high cytotoxicity-low cytokine’ phenotype and may act to suppress viral reactivation whilst minimizing tissue inflammation. Improved understanding of the physiological role of PD-1 will help to delineate the mechanisms, and potential reversal, of PD-1+ CD4+ T cell exhaustion in patients with malignant disease.

2021-02-16 | GSE165952 | GEO

PD-1 is imprinted on cytomegalovirus-specific CD4+ T cells and attenuates Th1 cytokine production whilst maintaining cytotoxicity.

Project description:PD-1 is expressed on exhausted T cells in cancer patients but its physiological role remains uncertain. We determined the phenotype, function and transcriptional correlates of PD-1 expression on cytomegalovirus-specific CD4+ T cells during latent infection. PD-1 expression ranged from 10-85% and remained stable over time within individual donors. This 'setpoint' was correlated with viral load at primary infection. PD-1+ CD4+ T cells display strong cytotoxic function but generate low levels of Th1 cytokines which is only partially reversed by PD-1 blockade. TCR clonotypes showed variable sharing between PD-1+ and PD-1- CMV-specific cells indicating that PD-1 status is defined either during T cell priming or subsequent clonal expansion. Physiological PD-1+ CD4+ T cells therefore display a unique 'high cytotoxicity-low cytokine' phenotype and may act to suppress viral reactivation whilst minimizing tissue inflammation. Improved understanding of the physiological role of PD-1 will help to delineate the mechanisms, and potential reversal, of PD-1+ CD4+ T cell exhaustion in patients with malignant disease.

| S-EPMC7963093 | biostudies-literature

Th1/Th17 cell associated pathways are upregulated in murine cytomegalovirus infected murine kidneys after allogeneic transplantation

Project description:Th1/Th17 cell associated pathways are upregulated in murine cytomegalovirus infected murine kidneys after allogeneic transplantation

| PRJNA744942 | ENA

Decoding murine cytomegalovirus

Project description:Decoding murine cytomegalovirus

| PRJNA874807 | ENA

Fatty acids reshape the cytotoxicity and epigenetics of tumor-resident CD8+ T cells by maintaining SCML4 expression

Project description:Fatty acids reshape the cytotoxicity and epigenetics of tumor-resident CD8+ T cells by maintaining SCML4 expression

| PRJNA883624 | ENA

Impact of Acute methionine restriction on proteome of Th1 cells - Part 2

Project description:CD4 T cells were activated using CD3/CD28 antibodies in the presence of IL2 and IL12, to generate Th1 cells. Th1 cells were maintained and expanded in IL2 and IL12, on D5 Th1 cells were sorted for CD4+ expression and DAP1 exclusion. After flow sorting, live TH1 cells were resuspended (1e6 per ml) in methionine free RPMI, supplemented with 10% dialysed FBS, IL2 and IL12, and with L-methionine (100μM, or 1μM). Cells were cultured for 5 hrs before collection for proteomics processing.

2019-03-29 | PXD012053 | Pride

P2X7 signaling drives Th1 cell differentiation through metabolic reprogramming for aerobic glycolysis

Project description:This study provides evidence on the molecular mechanisms by which P2RX7 signaling promotes Th1 cell differentiation. P2RX7 induces T-bet expression and aerobic glycolysis in splenic CD4+ T cells that respond to malaria, at a time prior to Th1/Tfh polarization. Cell-intrinsic P2RX7 signaling sustains the glycolytic pathway and causes bioenergetic mitochondrial stress in activated CD4+ T cells. We also show in vitro the phenotypic similarities of Th1-polarized CD4+ T cells that do not express P2RX7 and those in which the glycolytic pathway is pharmacologically inhibited. In addition, ATP synthase blockade in vitro and the consequent inhibition of oxidative phosphorylation, which forces cells to use aerobic glycolysis, is sufficient to promote rapid CD4+ T cell proliferation and polarization to the Th1 profile in the absence of P2RX7. These data demonstrate that P2RX7-mediated metabolic reprograming for aerobic glycolysis is a key event for Th1 cell differentiation and suggest that ATP synthase inhibition is a fundamental mechanism by which P2X7 signaling induces the Th1 response.

2023-03-08 | PXD037754 | Pride

CXCR3+ Treg cells suppress Th1-immune responses through expression of the co-inhibitory receptors CD85k and Lag-3

Project description:CD4+Foxp3+ Treg cells are essential for maintaining self-tolerance and preventing excessive immune responses. In the context of Th1 immune responses, co-expression of the Th1 transcription factor T-bet with Foxp3 is essential for Treg cells to control Th1 responses. T-bet-dependent expression of CXCR3 directs Tregs to the site of inflammation, however, the suppressive mediators enabling effective control of Th1 responses at this site are unknown. In this study, we determined the signature of CXCR3+ Treg cells arising in Th1 settings and defined universal features of Treg cells in this context using multiple Th1-dominated models. Our analysis defined a set of Th1-specific co-inhibitory receptors that are specifically expressed in Treg cells during Th1 immune responses. Among these, we identified the novel co-inhibitory receptor CD85k as a functional mediator of the enhanced suppression of Th1 effector cells by CXCR3+ Treg cells.

2018-06-30 | E-MTAB-6156 | biostudies-arrayexpress

Murine Cytomegalovirus research reagents

Project description:Murine Cytomegalovirus pSM3fr

| PRJEB64494 | ENA

Th1/Th17 cell associated pathways are upregulated in murine cytomegalovirus infected murine kidneys after allogeneic transplantation

Project description:Purpose: To characterize transcriptional profiles of murine cytomegalovirus infected allografts after renal transplantation. Methods: RNA was isolated from murine allografts and native kidneys, with and without MCMV infection. Libraries were generated and paired end 150 base pair sequencing was performed on the HiSeq 4000 (Illumina) (Supplementary Methods). Each sample was aligned to the GRCm38.p4 assembly of the mouse reference from NCBI using version 2.6.0c of the RNA-Seq aligner STAR. Transcript features were identified from the GFF file provided with the assembly from NCBI and raw coverage counts were calculated using HTSeq. The raw RNA-Seq gene expression data was normalized and post-alignment statistical analyses were performed using DESeq2 and custom analysis scripts written in R. Comparisons of gene expression and associated statistical analysis were made between different conditions of interest using the normalized read counts. All fold change values are expressed as test condition/control condition, where values less than 1 are denoted as the negative of its inverse. Results: The QIAGEN Ingenuity Pathway Analysis (IPA) software was used for canonical pathway and differential gene expression analyses. IPA showed that, compared to MCMV infected native kidneys, transplantation of MCMV-infected kidneys led to significant changes in 5502 genes (adjusted p values <0.05), involved in 391 canonical pathways. The Th17 activation pathway showed 107 differentially expressed genes.Th1 pathway was one of the most highly upregulated pathways observed in the MCMV infected allografts. Conclusions: Transcripts for Th1/Th17 cell associated activation and signaling are differentially expressed in MCMV infected kidneys after allogeneic transplantation.

2021-07-15 | GSE179788 | 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