Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Effector Memory T cells induce DC-intrinsic DNA damage and a non-canonical STING pathway during innate inflammation [ATAC]

ABSTRACT: Effector Memory T cells induce DC-intrinsic DNA damage and a non-canonical STING pathway during innate inflammation [ATAC]

PROVIDER: PRJNA953400 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR24108283_1.fastq.gz	Fastqsanger.gz
	SRR24108283_2.fastq.gz	Fastqsanger.gz
	SRR24108284_1.fastq.gz	Fastqsanger.gz
	SRR24108284_2.fastq.gz	Fastqsanger.gz
	SRR24108285_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 24

Similar Datasets

Effector Memory T cells induce DC-intrinsic DNA damage and a non-canonical STING pathway during innate inflammation

Project description:Effector Memory T cells induce DC-intrinsic DNA damage and a non-canonical STING pathway during innate inflammation

| PRJNA950996 | ENA

Effector Memory T cells induce DC-intrinsic DNA damage and a non-canonical STING pathway during innate inflammation

Project description:A breach in tolerance to self-antigens induces expansion of autoreactive T cells, ultimately leading to autoimmune inflammation. While autoreactive T cells are principal drivers of autoimmunity, tissue pathology is alternatively driven by innate cytokines, indicating that autoreactive T cells can induce innate inflammation. This study has led to the discovery that effector memory T (Tem) cells trigger double stranded breaks via mitochondrial ROS production in interacting DCs. Consequently, initiation of the DNA damage response leads to activation of a cGAS-independent, STING-TRAF6-NFkB signaling axis. STING deficient DCs display significant defects in transcriptional induction and functional production of IL-1b and IL-6 following their interaction with Tem cells, both in vitro and in vivo. The discovery of Tem induced innate inflammation through DNA damage and a non-canonical STING-mediated NFkB activation presents this pathway as a potential target to alleviate T cell driven autoimmune inflammation.

2023-10-03 | GSE228682 | GEO

Effector Memory T cells induce DC-intrinsic DNA damage and a non-canonical STING pathway during innate inflammation [ATAC]

2023-10-03 | GSE229204 | GEO

The tumor suppressor kinase DAPK3 drives tumor-intrinsic immunity through the STING-IFNb pathway Phospho

Project description:Phosphoproteomics show that the tumor suppressor kinase DAPK3 drives tumor-intrinsic immunity through the STING-IFNb pathway

2021-01-15 | MSV000086706 | MassIVE

Intrinsic self-DNA triggers inflammatory disease dependent on STING (I)

Project description:Inflammatory diseases such as Aicardi-Goutieres Syndrome (AGS) and severe systemic lupus erythematosus (SLE) are generally lethal disorders that have been traced to defects in the exonuclease Trex1 (DNAseIII). Mice lacking Trex1 similarly die at an early age through comparable symptoms, including inflammatory myocarditis, through chronic activation of the STING (stimulator of interferon genes) pathway. Here we demonstrate that phagocytes rather than myocytes are predominantly responsible for causing inflammation, an outcome that could be alleviated following adoptive transfer of normal bone marrow into Trex1-/- mice. Trex1-/- macrophages did not exhibit significant augmented ability to produce pro-inflammatory cytokines compared to normal macrophages following exposure to STING-dependent activators, but rather appeared chronically stimulated by genomic DNA. These results shed molecular insight into inflammation and provide concepts for the design of new therapies. Total RNA obtained from wild type (WT), Trex1 deficient (TKO), STING deficient (SKO), or Trex1 and STING double deficient (STKO) mouse Heart

2014-07-09 | E-GEOD-59217 | biostudies-arrayexpress

RNASeq analysis of solid tumours from CT26 syngeneic mice to study the role of T-cells and tumour intrinsic pathways (STING/IFN) for driving ceralasertib (AZD6738) efficacy

Project description:Understanding MoA of ceralasertib (AZD6738) in driving efficacy through immune regulation via T-cells and tumour intrinsic pathways (STING/IFN) for AZD6738 driven efficacy.

2024-01-29 | E-MTAB-13703 | biostudies-arrayexpress

The tumor suppressor kinase DAPK3 drives tumor-intrinsic immunity through the STING-IFNb pathway Proteome

Project description:Proteome analysis reveals that the tumor suppressor kinase DAPK3 drives tumor-intrinsic immunity through the STING-IFNb pathway Proteome

2021-01-15 | MSV000086708 | MassIVE

Intrinsic self-DNA triggers inflammatory disease dependent on STING (II)

Project description:Inflammatory diseases such as Aicardi-Goutieres Syndrome (AGS) and severe systemic lupus erythematosus (SLE) are generally lethal disorders that have been traced to defects in the exonuclease Trex1 (DNAseIII). Mice lacking Trex1 similarly die at an early age through comparable symptoms, including inflammatory myocarditis, through chronic activation of the STING (stimulator of interferon genes) pathway. Here we demonstrate that phagocytes rather than myocytes are predominantly responsible for causing inflammation, an outcome that could be alleviated following adoptive transfer of normal bone marrow into Trex1-/- mice. Trex1-/- macrophages did not exhibit significant augmented ability to produce pro-inflammatory cytokines compared to normal macrophages following exposure to STING-dependent activators, but rather appeared chronically stimulated by genomic DNA. These results shed molecular insight into inflammation and provide concepts for the design of new therapies. Total RNA obtained from wild type murine embryonic fibroblasts (WT MEFs), Trex1 deficient MEFs (TKO) or STING and Trex1 double deficient MEFs (STKO) transfected with or without double strand DNA 90 (ISD) and examined cytokine production by these cells.

2014-07-09 | E-GEOD-59218 | biostudies-arrayexpress

Intrinsic self-DNA triggers inflammatory disease dependent on STING

Project description:Intrinsic self-DNA triggers inflammatory disease dependent on STING

| PRJNA254744 | ENA

RNASeq analysis of Myeloid Derived Suppressor Cells (MDSCs) from MC38 syngeneic mice to study their role on tumour intrinsic pathways (STING/IFN) for driving ceralasertib (AZD6738) efficacy

Project description:Understanding MoA of ceralasertib (AZD6738) in driving efficacy through immune regulation via polymorphonuclear-myeloid derived suppressor cells (PMN-MDSC) and monocytic-myeloid derived suppressor cells (M-MDSC) on tumour intrinsic pathways (STING/IFN) for AZD6738 driven efficacy. Animals were treated only for 7 days and left for further 7 days without treatment. We compared cells against Vehicle and spleen derived ( naive) as a positive control.

2024-01-30 | E-MTAB-13707 | biostudies-arrayexpress

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