Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Reduced CD8 T cell exhaustion in DR4 risk subjects is selectively augmented with therapy [CD8s]

ABSTRACT: Reduced CD8 T cell exhaustion in DR4 risk subjects is selectively augmented with therapy [CD8s]

PROVIDER: PRJNA894958 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR22063316.fastq.gz	Fastqsanger.gz
	SRR22063317.fastq.gz	Fastqsanger.gz
	SRR22063318.fastq.gz	Fastqsanger.gz
	SRR22063319.fastq.gz	Fastqsanger.gz
	SRR22063320.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 40

Similar Datasets

Reduced CD8 T cell exhaustion in DR4 risk subjects is selectively augmented with therapy.

Project description:Reduced CD8 T cell exhaustion in DR4 risk subjects is selectively augmented with therapy.

| PRJNA894952 | ENA

Reduced CD8 T cell exhaustion in DR4 risk subjects is selectively augmented with therapy [whole blood]

Project description:Reduced CD8 T cell exhaustion in DR4 risk subjects is selectively augmented with therapy [whole blood]

| PRJNA894957 | ENA

Reduced CD8 T cell exhaustion in DR4 risk subjects is selectively augmented with therapy [CD8s]

Project description:Exhausted CD8 T cells (TEX) are associated with worse outcome in cancer yet better outcome in autoimmunity. However, factors contributing to reduced TEX in autoimmunity are poorly understood. We use two genetically related autoimmune diseases, type 1 diabetes (T1D) and rheumatoid arthritis (RA), to explore these factors. We identify a common human peripheral blood TIGIT+KLRG1+ CD8 TEX population: TIGIT+KLRG1+ CD8 TEX of healthy controls (HC), T1D, and rheumatoid arthritis (RA) subjects share EOMES signature genes, are increased with age and in chronic viral-specific cells and are hyporesponsive in vitro. Consistent with a genetic determinant, TIGIT+KLRG1+ TEX are stable within but vary between individuals. In HC and RA subjects (n>100/cohort), lower levels of EOMES transcriptional modules and TIGIT+KLRG1+ TEX were associated with RA HLA risk alleles (DR0401, 0404, 0405, 0408, 1001) even when considering disease status and CMV seropositivity. TIGIT+KLRG1+ TEX significantly increased in RA HLA risk but not non-risk subjects treated with abatacept (CTLA4Ig); no change in TIGIT+KLRG1+ TEX was observed with adalimumab (anti-TNF) therapy. The DR4 association and selective modulation with abatacept suggests that therapeutic modulation of TEX may be more effective in DR4 subjects and TEX may be indirectly influenced by cellular interactions that are blocked by abatacept.

2023-06-30 | GSE216679 | GEO

Reduced CD8 T cell exhaustion in DR4 risk subjects is selectively augmented with therapy [whole blood]

2023-06-30 | GSE216678 | GEO

Reduced CD8 T cell exhaustion in DR4 risk subjects is selectively augmented with therapy.

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

2023-06-30 | GSE216680 | GEO

Transcriptome differences in HCC infiltrated CD8+ T cells in effector and exhaustion state

Project description:CD8+ T cells isolated from HCC tissue were divided into three groups: PD1-TIM3- CD8+ TILs, exhibiting full effector function; PD1-intTIM3+ CD8+ TILs, exhibiting partial exhaustion; and PD1-hiTIM3+ CD8+ TILs, exhibiting severe exhaustion, as reflected by the differences in their ability to produce effector cytokines respectively. Transcriptome sequence analysis was performed to investigate the gene expression profile was performed.

2019-12-31 | E-MTAB-7278 | biostudies-arrayexpress

Multiomic profiling of chronically activated CD4+ T cells identifies drivers of exhaustion and metabolic reprogramming

Project description:T-cell exhaustion occurs when T cells are chronically activated, usually in the context of cancer or chronic infection. Exhausted T cells lose effector functions, upregulate inhibitory receptors, and lose proliferation ability. Understanding the mechanisms of T-cell exhaustion is important as it has critical clinical applications, such as checkpoint blockade therapy. CD4+ T cells are understudied in the context of exhaustion, and no large-scale multiomic datasets containing proteomics, phosphoproteomics, or metabolomics exist. We therefor performed a multiomic experiment to profile this cell state using a time course analysis to also capture progression.

2024-11-28 | PXD057703 | Pride

Ulcerative Colitis subjects

Project description:Ulcerative Colitis subjects

| PRJNA420680 | ENA

Lymphopenia-induced T cell exhaustion in STING gain-of-function mouse model

Project description:STING gain-of-function (GOF) mutations lead to T cell lymphopenia, in the context of severe combined immunodeficiency (SCID) for STING GOF V154M mice. This T cell lymphopenia, which is of central origin, has been described as type I IFN independent and associated with dysfunctions of the rare mature T cells found in the periphery. To better describe the biological mechanisms of these dysfunctions, we performed a transcriptomic analysis by RNA-seq on sorted splenic CD4+ and CD8+ mature T cells from STING GOF mice. We highlighted an unexpected T cell exhaustion phenotype that could partly explain their dysfunctions. Acquired very early in life, but only once the peripheral environment is reached, the phenotype appeared to depend neither on type I IFNs, nor on the intrinsic activation of STING in T or stromal cells. Mechanistically, the few mature T cells reaching the periphery seem to be rapidly impacted by the lymphopenic environment through increased antigenic and IL-7 stimulations that could lead to their exhaustion. By using STING GOF long term-hematopoietic stem cells (LT-HSC) transplantations with supportive wild-type bone marrow (BM) cells, we prevented the T cell exhaustion of STING GOF T cells in the resulting non lymphopenic context. With the support of lymphopenic RAG1 hypomorphic mice developing the phenotype, our data uncover a lymphopenia-mediated T cell exhaustion mechanism in STING GOF mice, for which a synergistic effect of the mutation is also envisaged.

2024-01-07 | E-MTAB-13658 | biostudies-arrayexpress

NFAT5 induction by the tumor microenvironment enforces CD8 T cell exhaustion [ATAC]

Project description:Persistent exposure to antigen during chronic infection or cancer renders T cells dysfunctional. The molecular mechanisms regulating this state of exhaustion are thought to be common in infection and cancer, despite obvious differences in their microenvironments. We discovered that NFAT5, an NFAT family member lacking an AP-1 docking site, is highly expressed in exhausted T cells responding to chronic infection and tumors but is a central player selectively in tumor-induced exhaustion. While NFAT5 overexpression in CD8+ T cells reduced tumor control, NFAT5 deletion improved tumor control by promoting the accumulation of tumor-specific CD8 T cells that expressed less TOX and PD-1 and produced more cytokines specifically among precursor exhausted cells. Conversely, NFAT5 did not promote T cell exhaustion during chronic infection. While NFAT5 expression was induced by TCR triggering, its transcriptional activity was specific to the tumor microenvironment and required hyperosmolarity. NFAT5 thus promotes CD8 T cell exhaustion in a tumor-selective fashion.

2023-07-23 | GSE237711 | 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