Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gut microbiota-specific IgA+ B cells traffic to the CNS in active multiple sclerosis

ABSTRACT: Gut microbiota-specific IgA+ B cells traffic to the CNS in active multiple sclerosis

PROVIDER: PRJEB40803 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Gut-microbiota specific IgA B cells traffic to the CNS in multiple sclerosis

Project description:Gut-microbiota specific IgA B cells traffic to the CNS in multiple sclerosis

| PRJEB32763 | ENA

Gut microbiota-specific IgA<sup>+</sup> B cells traffic to the CNS in active multiple sclerosis.

Project description: Not available

| S-EPMC8043673 | biostudies-literature

Bioinformatics Analyses Determined the Distinct CNS and Peripheral Surrogate Biomarker Candidates between Two Mouse Models for Progressive Multiple Sclerosis

Project description:Previously, we have established two distinct progressive multiple sclerosis (MS) models by induction of experimental autoimmune encephalomyelitis (EAE) with myelin oligodendrocyte glycoprotein (MOG) in two mouse strains. A.SW mice develop ataxia with antibody deposition, but no T cell infiltration, in the central nervous system (CNS), while SJL/J mice develop paralysis with CNS T cell infiltration. In this study, we determined biomarkers contributing to the heterogeneities of the two models. Using the CNS and spleen microarray transcriptome and cytokine data, we conducted computational supervised analyses (volcano plot, heat map, and pathway analysis) and unsupervised principal component analysis (PCA) with pattern matching analysis (PMA).

2019-04-09 | GSE99300 | GEO

Project description:Gut microbiota-specific IgA+ B cells traffic to the CNS in active multiple sclerosis

| PRJNA669809 | ENA

Mononuclear phagocyte phenotypes in a multiple sclerosis model

Project description:Mononuclear phagocytes are key regulators of both tissue damage and repair in neuroinflammatory conditions such as multiple sclerosis (MS). To examine divergent phagocyte phenotypes in the inflamed central nervous system (CNS) we introduce an in vivo imaging approach combined with RNAseq and proteomics that allows us to temporally and spatially resolve the evolution of phagocyte polarization in a murine MS model. We show that the initial pro-inflammatory polarization of phagocytes is established after spinal cord entry and critically depends on the compartment they enter. Guided by signals from the CNS environment individual phagocytes then switch their phenotype as lesions move from expansion to resolution. Our study thus provides a first real-time analysis of the temporo-spatial determinants and regulatory principles of phagocyte specification in the inflamed CNS.

2019-07-10 | PXD010245 | Pride

Identifying CNS-colonizing T cells as potential therapeutic targets to prevent progression of multiple sclerosis

Project description:Background: Multiple sclerosis (MS), an autoimmune disease of the central nervous system (CNS), can be suppressed in its early stages but eventually becomes clinically progressive and unresponsive to therapy. Here we investigate whether the therapeutic resistance of progressive MS can be attributed to chronic immune cell accumulation behind the blood brain barrier. Methods: We systematically track CNS-homing immune cells in the peripheral blood of 31 MS patients and 31 matched healthy individuals in an integrated analysis of 497,705 single cell transcriptomes and 355,433 surface protein profiles from 71 samples. Through spatial RNA-sequencing we localize these cells in post-mortem brain tissue of 6 progressive MS patients contrasted against 4 control brains (20 samples, 85,000 spot transcriptomes). Findings: We identify a specific pathogenic CD161+/LTB+ T cell population that resides in brains of progressive MS patients. Intriguingly, our data suggest that the colonization of the CNS by these T cells may begin earlier in the disease course, as they can be mobilized to the blood by usage of the integrin-blocking antibody natalizumab in relapsing-remitting MS patients. Conclusions: As a consequence, we lay the groundwork for a therapeutic strategy to deplete CNS-homing T cells before they can fuel treatment-resistant progression. Funding: This study was supported by funding from the University Medical Center Hamburg-Eppendorf, the Stifterverband für die Deutsche Wissenschaft, the OAK Foundation, Medical Research Council UK and Wellcome.

2021-02-16 | GSE144744 | GEO

Human brain tissues from healthy controls and multiple sclerosis patients

Project description:Multiple sclerosis (MS) is characterized by cell proliferation, migration and damage in various cell types in different CNS regions and causes disabilities related to distinct neurological pathways, such as walking, vision and cognition. Here, region-specific transcriptomic approach was used to determine changes in gene expression in five different CNS regions (hippocampus, frontal cortex, internal capsule, corpus callosum, and parietal cortex) in MS.

2019-04-29 | GSE123496 | GEO

Proteomic analysis in multiple sclerosis

Project description:To address the differential response of the CNS, proteomics was applied in experimental autoimmune encephalomyelitis (EAE) mice and cuprizone (CPZ) mice in two different CNS regions

2023-09-27 | PXD037019 | JPOST Repository

Inhibition of astrocytic DRD2 suppresses CNS inflammation in an animal model of multiple sclerosis

Project description:Inhibition of astrocytic DRD2 suppresses CNS inflammation in an animal model of multiple sclerosis

| PRJNA844329 | ENA

Sustained infiltration of neutrophils into the CNS results in increased demyelination in a viral-induced model of multiple sclerosis

Project description:Intracranial inoculation of the neuroadapted JHM strain of mouse hepatitis virus (JHMV) into susceptible strains of mice results in acute encephalomyelitis and chronic immune-mediated demyelination similar to the human demyelinating disease multiple sclerosis (MS). JHMV infection of transgenic mice in which expression of the neutrophil chemoattractant chemokine CXCL1 is under the control of a tetracycline-inducible promoter active within GFAP-positive cells results in sustained neutrophil infiltration in the central nervous system (CNS) that correlates with an increase in spinal cord demyelination. We used single cell RNA sequencing (scRNAseq) and flow cytometry to characterize molecular and cellular changes within the CNS associated with increased demyelination in transgenic mice compared to control animals. These approaches revealed the presence of activated neutrophils as determined by increased expression of mRNA transcripts associated with increased neutrophil effector functions, such as CD63, MMP9, S100a8, S100a9, and ASPRV1, as well as by altered neutrophil morphology and protein expression. Collectively, these findings reveal insight into changes in the profile of neutrophils associated with increased white matter damage in mice persistently infected with a neurotropic coronavirus.

2022-09-09 | GSE212852 | 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