Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression data of CNS T cells during EAE

ABSTRACT: In the absence of NR4A2 in T cells mice do not develop early acute EAE, but only a late chronic disease. We examined the mechanism by which NR4A2 can control the pathogencity of T cells in CNS autoimmune disease. To determine how NR4A2 is involved is involved in T cell pathology, we examined expression profiles of T cells during early and late diease in the presence or genetic CD4-specific absence of NR4A2.

ORGANISM(S): Mus musculus

PROVIDER: GSE72301 | GEO | 2015/08/25

SECONDARY ACCESSION(S): PRJNA293691

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Expression data of CNS T cells during EAE

Project description:In the absence of NR4A2 in T cells mice do not develop early acute EAE, but only a late chronic disease. We examined the mechanism by which NR4A2 can control the pathogencity of T cells in CNS autoimmune disease. To determine how NR4A2 is involved is involved in T cell pathology, we examined expression profiles of T cells during early and late diease in the presence or genetic CD4-specific absence of NR4A2. T cells infiltrating CNS tissues were isolated at peal acute EAE (D18) or during late,chronic EAE (D32). RNA expression was then analysed by genechip to determine the influence of NR4A2 in T cells on these disease stages

2015-08-25 | E-GEOD-72301 | biostudies-arrayexpress

EAE CNS Gene Expression

Project description:Gene expression in the CNS, comparing wild-type and TRPV1-/- mice with active EAE.

2012-08-03 | E-MEXP-3698 | biostudies-arrayexpress

Single-cell transcriptional profiling of Th17 cells, harvested at peak of disease in EAE from CNS [EAE-CNS-IL-17A/GFP+]

Project description:Extensive cellular heterogeneity exists within specific immune-cell subtypes classified as a single lineage, but its molecular underpinnings are rarely characterized at a genomic scale. Here, we use single-cell RNA-seq to investigate the molecular mechanisms governing heterogeneity and pathogenicity of Th17 cells isolated from the central nervous system (CNS) and lymph nodes (LN) at the peak of autoimmune encephalomyelitis (EAE) or polarized in vitro under either pathogenic or non-pathogenic differentiation conditions. Computational analysis reveals a spectrum of cellular states in vivo, including a self-renewal state, Th1-like effector/memory states and a dysfunctional/senescent state. Relating these states to in vitro differentiated Th17 cells, unveils genes governing pathogenicity and disease susceptibility. Using knockout mice, we validate four novel genes: Gpr65, Plzp, Toso and Cd5l (in a companion paper). Cellular heterogeneity thus informs Th17 function in autoimmunity, and can identify targets for selective suppression of pathogenic Th17 cells while sparing non-pathogenic tissue-protective ones. Single-cell transcriptional profiling of Th17 cells, harvested at peak of disease in EAE from CNS

2015-11-20 | E-GEOD-75107 | biostudies-arrayexpress

Transcriptome profiling of a backcross between experimental autoimmune encephalomyelitis (EAE)-susceptible DA and EAE-resistant PVG rat strains to identify expression quantitative trait loci.

Project description:The aim of the experiment is to characterize the genetics and mechanisms of the inflammatory response after induction of experimental autoimmune encephalomyelitis (EAE), a model of multiple sclerosis, by studying the genome wide expression in the spleen in late disease. A backcross was created between EAE-susceptible DA and EAE-resistant PVG rats. At day 35 after induction of EAE with myelin oligodendrocyte glycoprotein (MOG) in these rats, spleens were taken for transcriptional profiling.

2013-08-10 | E-MTAB-784 | biostudies-arrayexpress

Gene expression profiling of mouse experimental autoimmune encephalomyelitis (EAE) from spinal cord preparations of opticospinal EAE (OSE) and MOG-induced EAE

Project description:Genetic opticospinal EAE (OSE) and MOG-induced EAE (MOG-EAE) are two experimental autoimmune encephalomyelitis (EAE) mouse models of human multiple sclerosis. For the OSE model, double-transgenic 2D2 (TCRMOG) x IgHMOG mice were used. For MOG-EAE, wildtype C57BL/6 mice were immunized with a MOG peptide consisting of the amino acids 35-55, administered in complete Freund’s adjuvant containing 5mg / ml Mycobacterium tuberculosi. The severity of EAE was rated on the scale 0: healthy animal; 1: animal with a flaccid tail; [...]; 4: animal with both hind legs paralyzed. The case groups in the experiment were: OSE1: OSE with disease score 1; OSE4: OSE with disease score 4; MOG4: MOG-EAE injected with both MOG and adjuvant, with disease score 4. The control groups in the experiment were: OSE0: OSE with disease score 0; CFA: C57BL/6 mice injected only with adjuvant (no MOG); WT: Wildtype C57BL/6 mice. The aim of the experiment was to assess gene expression differences 1) between OSE4 and OSE0, 2) between OSE1 and OSE0, and 3) between MOG4 and CFA. For control, WT was compared to OSE0 and CFA. Subsequently, differentially expressed transcripts were compared, first, between the OSE4 vs. OSE0 and the MOG4 vs. CFA contrasts (different EAE models) and, second, between the OSE4 vs. OSE0 and the OSE1 vs. OSE0 contrasts (different EAE severity).

2020-08-21 | E-MTAB-9132 | biostudies-arrayexpress

Comparative genomic hybridization of experimental autoimmune encephalomyelitis (EAE)-susceptible DA and EAE-resistant PVG rat strains stimulated with myelin oligodendrocyte glycoprotein (MOG) to identify the alternative splicing.

Project description:Experimental autoimmune encephalomyelitis (EAE)-susceptible DA and EAE-resistant PVG rats were immunized with myelin oligodendrocyte glycoprotein (MOG) to induce an autoimmune response.<br>Seven days later draining inguinal lymph nodes were removed. 2 conditions were examined: 'ex vivo' and 'MOG restimulated', which involved 24hrs of incubation with an encephalogenic MOG 91-108 peptide.

2009-11-01 | E-MEXP-2237 | biostudies-arrayexpress

Pharmacologic or genetic inhibition of EphB3 receptor kinase impacts CNS pathology during progressive EAE

Project description:We evaluated the role of EphB3 on the regulation of astrocyte and microglial responses and its potential as a therapeutic target during progressive EAE. We induced EAE in NOD mice that will develop a progressive form of the disease. Starting at the beginning of the progressive phase, A38 was administered and alternatively EphB3 was KD in astrocytes. Both treatments ameliorated the EAE. The transcriptional analysis of astrocytes and microglia revealed the decreased expression of genes associated to inflammation and neurodegeneration in both conditions.

2022-02-25 | GSE149105 | GEO

Transcriptome analysis of CNS and splenic FOXP3+ Tregs vs. exFOXP3 T cells during EAE

Project description:EAE was induced in female FOXP3 fate mapping mice. At peak of disease, immune cells were isolated from brain and spinal cord (pooled as CNS) and spleen. Next, FOXP3+ and exFOXP3 T cells were FACS-sorted based on RFP and GFP expression.

2024-02-16 | GSE255607 | GEO

Population transcriptional profiling of Th17 cells, isolated from CNS or LN at peak of disease in EAE

Project description:Extensive cellular heterogeneity exists within specific immune-cell subtypes classified as a single lineage, but its molecular underpinnings are rarely characterized at a genomic scale. Here, we use single-cell RNA-seq to investigate the molecular mechanisms governing heterogeneity and pathogenicity of Th17 cells isolated from the central nervous system (CNS) and lymph nodes (LN) at the peak of autoimmune encephalomyelitis (EAE) or polarized in vitro under either pathogenic or non-pathogenic differentiation conditions. Computational analysis reveals a spectrum of cellular states in vivo, including a self-renewal state, Th1-like effector/memory states and a dysfunctional/senescent state. Relating these states to in vitro differentiated Th17 cells, unveils genes governing pathogenicity and disease susceptibility. Using knockout mice, we validate four novel genes: Gpr65, Plzp, Toso and Cd5l (in a companion paper). Cellular heterogeneity thus informs Th17 function in autoimmunity, and can identify targets for selective suppression of pathogenic Th17 cells while sparing non-pathogenic tissue-protective ones. Population transcriptional profiling of Th17 cells, isolated from CNS or LN at peak of disease in EAE

2015-11-20 | E-GEOD-75105 | biostudies-arrayexpress

Farnesol brain transcriptomics in CNS inflammatory demyelination

Project description:To understand the molecular mechanisms underlying the protective neuroinflammatory activity of farnesol (FOL), we examined the transcriptomic profile of the brains of EAE mice treated with daily oral FOL using next-generation sequencing (RNA-seq). EAE-induced mice, compared to naïve, healthy mice, overall showed increased expression in pathways for immune response, as well as increased cytokine signaling pathway, with downregulation of cellular stress proteins. Our analysis found that FOL downregulated pro-inflammatory pathways and attenuated the immune response in EAE. FOL downregulated the expression of genes involved in misfolded protein response, MAPK activation/signaling, and pro-inflammatory response.

2023-09-11 | GSE233583 | GEO

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