Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

10 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Disease-Associated SNPs From non-Coding Regions in Juvenile Idiopathic Arthritis Are Located Within or Adjacent to Functional Genomic Elements of Human Neutrophils and CD4+ T Cells [RNA-Seq]

ABSTRACT: We sequenced mRNA from 3 neutrophil cells taken from 3 male adult to generate the gene expression profile of human neutrophil cells Examination of mRNA levels in human neutrophils.

ORGANISM(S): Homo sapiens

SUBMITTER: Lisha Zhu

PROVIDER: E-GEOD-66895 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Disease-Associated SNPs From non-Coding Regions in Juvenile Idiopathic Arthritis Are Located Within or Adjacent to Functional Genomic Elements of Human Neutrophils and CD4+ T Cells [ChIP-Seq]

Project description:We applied ChIP-Seq on two histone marks: H3K4me1 and H3K27ac in healthy human neutrophils. After peak calling, we obtained the peak regions enriched with H3K4me1 and H3K27ac histone marks and identifed aciive enhancers (H3K27ac+/H3K4me1+) and H3K27ac active enhancers (H3K27ac+/H3K4me1-) in human neutrophils and checked whether those enhancers are located in the LD blocks of 22 SNPs associtated with Juvenile Idiopathic Arthritis. Identification of active enhancers in human neutrohils

2015-06-12 | E-GEOD-66896 | biostudies-arrayexpress

Disease-Associated SNPs From non-Coding Regions in Juvenile Idiopathic Arthritis Are Located Within or Adjacent to Functional Genomic Elements of Human Neutrophils and CD4+ T Cells

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2015-06-12 | E-GEOD-66898 | biostudies-arrayexpress

Microarray study using whole blood and purified leucocyte populations from healthy controls and patients with tuberculosis or sarcoidosis with tuberculosis and sarcoidosis

Project description:Whole blood and purified leucocyte populations were compared to determine which cell types the whole blood interferon-inducible signature, found in both tuberculosis and sarcoidosis, was present in. This study agreed with previous publication that the neutrophil was the dominant cell in tuberculosis and also showed it was the dominant cell type in sarcoidosis. There were 5 patients in each group of healthy controls, tuberculosis and sarcoidosis. The cell types were whole blood, PBMCs, monocytes (CD14), T cells (CD8 and CD4) and neutrophils (CD15).

2013-10-31 | E-GEOD-42832 | biostudies-arrayexpress

Gene Expression Profiles Distinguish Children with Inactive Polyarticular Juvenile Idiopathic Arthritis (JIA) with a Predilection to Flare

Project description:Gene expression profiles were obtained from 17 children with rheumatoid factor negative (RF-) polyarticular juvenile idiopathic arthritis (JIA). The disease was inactive in all patients at visit 1. Thee disease remained inactive at visit 2 for 9 patients, while the other 8 patients were experiencing a disease flare at visit 2. The goal of the study was to better understand the underlying molecular biology of flares in JIA Total RNA was obtained from PBMC at two different times in the course of disease 2 samples from each of 17 patients were collected and analyzed different times in the course of the disease

2013-12-14 | E-GEOD-26112 | biostudies-arrayexpress

Transcriptome analysis of CD16/CD62L neutrophil subsets during human experimental endotoxemia

Project description:During systemic inflammation, different neutrophil subsets are mobilized to the blood circulation. These neutrophil subsets can be distinguished from normal circulating neutrophils (CD16bright/CD62Lbright) based on either an immature CD16dim/CD62Lbright or a CD16bright/CD62Ldim phenotype. Interestingly, the latter neutrophil subset is known to suppress lymphocyte proliferation ex vivo, but the underlying mechanism is largely unknown. We performed transcriptome analysis on the different neutrophil subsets to identify changes that are relevant for their functions. Neutrophil subsets were isolated by FACS sorting from the blood of healthy volunteers who were administered a single dose of lipopolysaccharide (LPS). The transcriptome was determined by microarray. The mobilized neutrophil subsets were characterized by specific transcriptome profiles reflecting their phase in neutrophil lifespan. Interestingly, the CD16bright/CD62Ldim suppressive neutrophils showed an interferon-induced transcriptome profile. This was confirmed by stimulation of peripheral neutrophils with IFNgamma. These cells acquired the capacity to suppress lymphocyte proliferation through the expression of programmed death ligand 1 (PD-L1). These data demonstrate that the suppressive phenotype of the neutrophil subset is induced by IFNgamma. Specific stimulation of neutrophils might have a pivotal role in regulating lymphocyte-mediated inflammation and autoimmune disease. After LPS infusion, blood was taken at t=0 and t=4 hours. Neutrophils were FACS sorted based on CD16 and CD62L expression. Gene expression of neutrophil subsets was assessed relative to t=0 as control.

2013-05-01 | E-GEOD-42358 | biostudies-arrayexpress

RNA-seq of bone marrow neutrophils from wild-type mice (C57BL/6) and CD40LG knockout mice.

Project description:We aimed to investigate the effect of CD40L on neutrophil development by comparing the transcription profile of wild-type and knockout mice. Thus, we performed RNA-sequencing of bone marrow neutrophils from wild-type mice (C57BL/6) and CD40LG knockout mice.

2021-08-07 | E-MTAB-10732 | biostudies-arrayexpress

Accurate MS-based Rab10 phosphorylation stoichiometry determination as readout for LRRK2 activity in Parkinson’s disease

Project description:Pathogenic mutations in the Leucine-rich repeat kinase 2 (LRRK2) are the predominant genetic cause of Parkinson’s disease (PD). They increase its activity, resulting in augmented Rab10-Thr73 phosphorylation and conversely, LRRK2 inhibition decreases pRab10 levels. Monitoring pRab10 can thus serve as a readout for LRRK2 activity; however, no sufficiently accurate assay to quantify pRab10 levels for drug target engagement or patient stratification exists. Here, we developed an ultra-sensitive targeted mass spectrometry (MS)-based assay for determining Rab10-Thr73 phosphorylation stoichiometry in human samples. It uses synthetic stable isotope-labeled (SIL) analogues for both phosphorylated and non-phosphorylated tryptic peptides surrounding Rab10-Thr73 to directly derive the percentage of Rab10 phosphorylation from attomole amounts of the endogenous phosphopeptide. We test the reproducibility of our assay by determining Rab10-Thr73 phosphorylation stoichiometry in human neutrophils before and after LRRK2 inhibition. Compared to healthy controls, neutrophils of LRRK2 G2019S and VPS35 D620N carriers robustly display 1.4-fold and 3.7-fold increased pRab10 levels, respectively. Our generic MS-based assay further establishes the relevance of pRab10 as a prognostic PD marker and is a powerful tool for determining LRRK2 inhibitor efficacy and for stratifying PD patients for LRRK2 inhibitor treatment.

2020-07-03 | PXD015219 | Pride

Semi-quantitative proteomics enables mapping of global neutrophil dynamics following influenza virus infection

Project description:Lung neutrophils are causally associated with IAV-induced disease severity. Less is known about the repertoire of lethal IAV-associated neutrophil proteins or about how global changes in different neutrophil compartments are coordinated following lethal IAV infection. Here, we use semi-quantitative proteomics to characterize dynamic alterations in BM, blood and lung neutrophils at homeostasis or following a lethal IAV infection, with a secondary aim of identifying lung neutrophil-derived proteins which are selectively induced following IAV infection. Our findings identify bone marrow neutrophil maturation as the key site of anti-viral activity induction, with further upregulation or release of both anti-viral and antimicrobial effectors occurring following lung tissue infiltration.

2019-05-29 | PXD012681 | Pride

Transcription profiling of CD14 monocytyes and CD16 neutrophils from patients with systemic lupus erythematosus

Project description:Copy number variation (CNV) has been shown to be common in regions of the genome coding for immune-related genes, and thus impacts upon polygenic autoimmunity. Low copy number of FCGR3B has recently been associated with systemic lupus erythematosus (SLE). FcγRIIIb is a glycosylphosphatidylinositol-linked, low affinity receptor for IgG found predominantly on human neutrophils. We present novel data demonstrating that both in a family with FcγRIIIb-deficiency, and in the normal population, FCGR3B CNV correlates with protein expression, with neutrophil uptake of and adherence to immune complexes, and with soluble serum FcγRIIIb. Reduced FcγRIIIb expression is thus likely to contribute to the impaired clearance of immune complexes which is a feature of SLE, explaining the association between low FCGR3B CNV and SLE that we have confirmed in a Caucasian population. In contrast, anti-neutrophil cytoplasmic antibody -associated vasculitis (AASV), a disease not associated with immune complex deposition, is associated with high FCGR3B CN. Thus we define a role for FCGR3B CNV in immune complex clearance, a function which may explain why low FCGR3B CNV is associated with SLE but not AASV. This is the first report of an association between disease-related gene CNV and variation in protein expression and function that may contribute to autoimmune disease susceptibility.

2008-10-02 | E-TABM-463 | biostudies-arrayexpress

Expression data from control, aged and activated neutrophils in mouse blood

Project description:Neutrophils provide immune protection against pathogens but also may promote tissue injury in inflammatory diseases. Although neutrophils are generally considered as a relatively homogeneous population, evidence for heterogeneity is emerging. Under steady-state conditions, neutrophil heterogeneity may arise from ageing and the replenishment by newly released neutrophils from the bone marrow. We used microarray to globally analyze gene expression in aged neutrophils and characterize the inflammatory programs that are activated during the aging process in the circulation. Control, aged and activated neutrophils were sorted directly from mouse blood for RNA extraction and hybridization on Affymetrix microarrays. We transfused whole blood and harvested donor neutrophils marked by the CD45.1 allele 6h later to derive neutrophils that had truly aged in vivo. Sorted neutrophils were compared to control donor neutrophils that had been transferred for only 10 min. Additionally, we harvested circulating neutrophils from TNF-? treated mice for comparison with neutrophils activated by systemic inflammation.

2015-09-24 | E-GEOD-69886 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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