Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

IL-6 driven pSTAT1 response is linked to T cell features implicated in early immune dysregulation

ABSTRACT: IL-6 driven pSTAT1 response is linked to T cell features implicated in early immune dysregulation

PROVIDER: PRJNA828611 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR18841400.fastq.gz	Fastqsanger.gz
	SRR18841401.fastq.gz	Fastqsanger.gz
	SRR18841402.fastq.gz	Fastqsanger.gz
	SRR18841403.fastq.gz	Fastqsanger.gz
	SRR18841404.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 96

Similar Datasets

IL-6 driven pSTAT1 response is linked to T cell features implicated in early immune dysregulation

Project description:Here, we performed an in-depth characterization of the effect of classic IL-6 signaling in primary human T cells from healthy individuals. We generated a detailed map of IL-6 signaling in CD4+ and CD8+ naïve and memory T cell subsets, linking mbIL-6R expression levels to the magnitude and balance of phosphorylation of STAT1 and STAT3 and the transcriptomics response to IL-6 in these subsets.

2022-06-27 | GSE201180 | GEO

IL-6-Driven pSTAT1 Response Is Linked to T Cell Features Implicated in Early Immune Dysregulation.

Project description: Not available

| S-EPMC9327741 | biostudies-literature

TDP-43 dysregulation impairs cholesterol metabolism linked with myelination defects

Project description:TDP-43 dysregulation impairs cholesterol metabolism linked with myelination defects

| PRJNA1248782 | ENA

Cellular and Extracellular microRNA Dysregulation in LRRK2-Linked Parkinson’s Disease

Project description:Cellular and Extracellular microRNA Dysregulation in LRRK2-Linked Parkinson’s Disease

| PRJNA1020167 | ENA

Interleukin-22 (IL-22) regulates B3GNT7 expression to induce intestinal fucosylation of O-linked glycans

Project description:Interleukin (IL) - 22 is a cytokine that plays a critical role in the maintenance of intestinal epithelial homeostasis. Its downstream functions are mediated through ligation of its heterodimeric receptor comprised of IL-22 receptor subunit alpha 1 (IL-22Ra1) and IL-10R2, and subsequent activation of signal transducer and activator of transcription 3 (STAT3). IL-22 signaling can induce genes necessary for intestinal epithelial cell proliferation, tissue regeneration, tight junction fortification, and production of antimicrobials. Emerging studies have also implicated IL-22 signaling in the regulation of intestinal epithelial fucosylation in mice. However, whether IL-22 regulates intestinal fucosylation in human intestinal epithelial cells and the molecular mechanisms that govern this process are unknown. Here, we show that IL-22 signaling regulates expression of the B3GNT7 transcript, which encodes a β1-3-N-acetylglucosaminyltransferase that can participate in the synthesis of poly-N-acetyllactosamine (LacNAc) chains. Additionally, we show that IL-22 signaling regulates levels of the a1-3-fucosylated Lewis X (Lex) blood group antigen and this glycan epitope is primarily displayed on heavily O-glycosylated intestinal epithelial glycoproteins. The IL-22-mediated increase in Lex antigen levels requires B3GNT7, as disruption of B3GNT7 expression moderated the IL-22-dependent increase in Lex antigen levels. Moreover, we show that increased expression of B3GNT7 alone is sufficient to promote increased display of Lex-decorated carbohydrate glycan structures primarily on O-glycosylated intestinal epithelial glycoproteins. Together, the data presented here identify B3GNT7 as a critical intermediary in IL-22-dependent induction of intestinal fucosylation of O-linked glycans and uncover a novel role for B3GNT7 in intestinal glycosylation.

2021-11-27 | GSE154889 | GEO

IMMUNE DYSREGULATION FOLLOWING INFECTION BY THE NEW CORONAVIRUS SARS-CoV-2 (COVID-19); A NEW DISEASE ENTITY

Project description:Severe pneumonia by the novel coronavirus (COVID-19 infection) is mediated through immune dysregulation. It was studied if this dysregulation persists after recovery and if it is linked to the manifestation of post-covid syndrome (PCS). Patients who had been hospitalized for COVID-19 pneumonia 3 to 6 months ago during two different time periods and matched comparators were the derivation cohort (n=46, September-October 2020) and the validation cohort (n=484, April-July 2021) respectively. Peripheral blood mononuclear cells (PBMCs) were isolated for culture and cytokine stimulation. Patients provided answers to two health questionnaires allowing classification into PCS and were also subject to lung function tests (LFT). The primary endpoint was the modulation of the production of interleukin (IL)-1b and IL-6 from monocytes and among secondary, the modulation of adaptive immune response and the development of PCS. Increased production of IL-1b (p<0.001) and IL-6 (p<0.001) was found in both study periods compared to control. There was increase of pro-inflammatory Th1 responses over anti-inflammatory Th2 responses and attenuation of the T17 response. PCS was manifested in 22% of patients, grouped into three groups of symptoms. Fatigue was associated with the predominance of Th2 responses and abnormal LFT with overproduction of IL-1b and IL-6. Immune dysregulation is apparent after three months post COVID-19 pneumonia with main features the hyper-production of IL-1β and IL-6 by circulating monocytes, the increase of the Th1/Th2 ratio and the attenuation of T17 response.

2025-06-05 | GSE206605 | GEO

Alzheimer's disease-related dysregulation of mRNA translation causes key pathological features with ageing

Project description:Alzheimer's disease-related dysregulation of mRNA translation causes key pathological features with ageing

| PRJNA642886 | ENA

Spatial transcriptomic mapping of canine osteosarcoma reveals immune microenvironment features linked to survival

Project description:Spatial transcriptomic mapping of canine osteosarcoma reveals immune microenvironment features linked to survival

| PRJNA1274825 | ENA

Context-dependent IL-1 mRNA-destabilization by TTP prevents dysregulation of immune homeostasis

Project description:Context-dependent IL-1 mRNA-destabilization by TTP prevents dysregulation of immune homeostasis

| PRJNA599384 | ENA

Proteomic analysis of platelets isolated from mice deficient for IL-33 or treated with recombinant IL-33

Project description:Platelets, traditionally recognized for their involvement in hemostasis and wound healing, also play a central role in immune regulation and inflammation. Their function and production adapt in response to inflammatory cues such as cytokines and danger-associated molecular patterns. Interleukin-33 (IL-33), an alarmin released during tissue damage, particularly in lung inflammation, has been implicated in influencing platelet biology, though its exact effects remain poorly understood. To clarify IL-33’s role, we examined its impact on platelet proteome. We first compared the proteome of platelets purified by FACS from IL-33-deficient (IL-33KO) mice versus WT mice (n=5 biological replicates in each group, 10 raw MS files). We also compared the proteome of platelets from WT mice which were either non stimulated (n= 8 biological replicates) or treated intranasally with recombinant IL-33 (n= 9 biological replicates).

2026-04-27 | PXD068068 | Pride

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