Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

EGAS00001003501-sc-20190311 - samples

ABSTRACT: We isolated T cells and monocotyes from healthy platelet donors and cultured them in resting and stimulated conditions with addition of a range of cytokines. We performed ATAC sequencing to assess the chromatin accessability in different cytokines treated cells. These cellular profiles were used to map risk variants to the cytokine-induced cell states relevant for autoimmune diseases. . This dataset contains all the data available for this study on 2019-03-11.

PROVIDER: EGAD00001004831 | EGA |

REPOSITORIES: EGA

ACCESS DATA

Json Xml

Similar Datasets

Chromatin accessability in cytokine induced immune cell states

Project description:We isolated T cells and monocotyes from healthy platelet donors and cultured them in resting and stimulated conditions with addition of a range of cytokines. We performed K27Ac ChM sequencing to assess the chromatin activity in different cytokines treated cells. These cellular profiles were used to map risk variants to the cytokine-induced cell states relevant for autoimmune diseases.

| EGAS00001002749 | EGA

Chromatin accessability in cytokine induced immune cell states

Project description:We isolated T cells and monocotyes from healthy platelet donors and cultured them in resting and stimulated conditions with addition of a range of cytokines. We performed ATAC sequencing to assess the chromatin accessability in different cytokines treated cells. These cellular profiles were used to map risk variants to the cytokine-induced cell states relevant for autoimmune diseases.

| EGAS00001003501 | EGA

EGAS00001002749-sc-2019-03-19T14:49:22Z - samples

| EGAD00001004852 | EGA

Gene epression regulation in cytokine induced immune cell states

| EGAS00001003823 | EGA

Single cell analysis of cytokine induced T cell states

Project description:We isolated T cells from healthy platelet donors and cultured them in resting and stimulated conditions with addition of a range of cytokines. We performed scRNA sequencing to assess the variability of polarization in different cytokines treated cells. Cytokines affect T cell responses by polarising them to different phenotypes. Given that the inflammation and and autoimmune tissue distruction is driven by the local production of cytokines, we investigated cytokine induced changes in T cells by using a combination of immunological and genomics approaches. To characterize, the efficacy of cytokine induced porization, here we stimulated naive and memory CD4+ T cells in the presence of cytokine polarizing coctails and profiled single cell transcriptome five days following polarization. This data is part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see http://www.sanger.ac.uk/datasharing/

| EGAS00001003215 | EGA

EGAS00001003215-sc-2019-08-27T13:29:54Z - samples

Project description:Cytokines affect T cell responses by polarising them to different phenotypes. We isolated T cells from healthy platelet donors and cultured them in resting and stimulated condition, as well as in the presence of Th2, iTreg and Th17 polarizing cocktail. To characterize the efficacy of cytokine induced porization and subpopulation specific response, we profiled single cell transcriptome five days following polarization using 10x platform (3' v2).

| EGAD00001005290 | EGA

EGAS00001003823-sc-2019-08-27T13:27:24Z - samples

Project description:Cytokines affect T cell responses by polarising them to different phenotypes. We isolated T cells from healthy platelet donors and cultured them in resting and stimulated conditions, as well as in the presence of Th1, Th2, Th17 and iTreg cocktail. In addition, T cells were stimulated in the presence of IL-10, IL-21, IL-27, IFNb and TNFa. We performed bulk RNA sequencing to assess impact of different disease-relevant cytokines upon T cell response.

| EGAD00001005291 | EGA

Haploinsufficiency in PTPN2 leads to early onset systemic autoimmunity from Evans syndrome to lupus

Project description:An exome sequencing strategy employed to identify pathogenic variants in patients with pediatric-onset systemic lupus or Evans syndrome resulted in the discovery of six novel monoallelic mutations in PTPN2. PTPN2 is a phosphatase that acts as an essential negative regulator of the JAK/STAT pathways downstream of several cytokine pathways. All identified mutations led to a loss of PTPN2 regulatory function as evidenced by in vitro cytokine reporter and phosphatase assays, and by hyperproliferation of patients’ T cells stimulated with cytokines. Furthermore, patients exhibited high serum levels of various inflammatory cytokines, mimicking the profile observed in individuals with gain-of-function mutations in various STAT factors. Flow cytometry analysis of patients’ blood cells revealed typical alterations associated with autoimmunity, such as an expansion of CD11c+ B cells and follicular helper T cells, and all patients presented with anti-platelet or other autoantibodies. These findings further supported the notion that a loss of function in negative regulators of cytokine pathways can lead to a broad spectrum of autoimmune manifestations and that PTPN2 along with SOCS1 haploinsufficiency constitute a new group of monogenic autoimmune diseases that can benefit from targeted therapy.

2024-06-21 | GSE270302 | GEO

NET proteome of neutrophils from people with long-standing type 1 diabetes and healthy control

Project description:Type 1 diabetes (T1D) is a chronic T-cell-mediated autoimmune disease, leading to the destruction of the pancreatic insulin-producing beta cells. Little is known about the involvement of neutrophils that exert multifaceted functions like phagocytosis, degranulation, production of cytokines and the formation of neutrophil extracellular traps (NETosis), in the pathogenesis of T1D. Our aim was to gain insight into the proteome of neutrophils undergoing NETosis from patients with long-standing T1D compared to age- and sex-matched healthy controls under both resting and stimulated conditions (phorbol-myristate acetate, PMA, 100nM; ionomycin, 20µM; 3hours) by LC/MS-MS.

2023-05-15 | PXD033599 | Pride

Lentiviral transduction of CD34+ cells induces genome-wide epigenetic modifications

Project description:Human CD34+ cells were cultured shortly in the presence of cytokines then with a gene transfer lentiviral vector (LV) expected to transduce cells but to have otherwise limited biological effects on the cells. At the end of the culture, the population of cells remained largely similar at the phenotypic level but some epigenetic changes were evident. Exposure of CD34+ cells to cytokines caused genome-wide DNA methylation changes. Surprisingly, the LV caused additional and distinct effects. Large-scale genomic DNA methylation analysis showed that balanced methylation changes occurred in about 200 genes following culture of CD34+ cells in the presence of cytokines but 900 genes were modified following addition of the LV, predominantly increasing CpG methylation. Epigenetic effects resulting from ex vivo culture and from the use of LV may constitute previously unsuspected sources of biological effects in stem cells and may provide new biomarkers to rationally optimize gene and cell therapy protocols. 3 replicates of control unstimulated (Group 1), cytokine stimulated, cytokine strimulated and treated with polybren and cytokine stimulated and transduced with lentiviral vector coding for GFP in the presence of polybren were analysed

2012-09-05 | E-GEOD-40631 | 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