Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Batf2 is a regulator of interferon gamma signaling in astrocytes during neuroinflammation

ABSTRACT: Batf2 is a regulator of interferon gamma signaling in astrocytes during neuroinflammation

PROVIDER: PRJNA1217491 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR32181918.fastq.gz	Fastqsanger.gz
	SRR32181919.fastq.gz	Fastqsanger.gz
	SRR32181920.fastq.gz	Fastqsanger.gz
	SRR32181921.fastq.gz	Fastqsanger.gz
	SRR32181922.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 5

Similar Datasets

Batf2 is a regulator of interferon gamma signaling in astrocytes during neuroinflammation

Project description:Astrocytic interferon (IFN)g signaling is associated with reduced neuroinflammation; however, downstream effectors responsible for regulating this protection are unknown. Here we identify an interferon-specific transcription factor, basic leucine zipper ATF-like transcription factor (BATF)2, that plays a key role in modulating the consequences of IFNg signaling in astrocytes. Chromatin immunoprecipitation (ChIP) sequencing revealed that BATF2 binds and prevents the overexpression of interferon regulatory factor (IRF)1 and IRF1 targets such as Caspase-1. We also show that Batf2-/- mice exhibit exacerbated clinical disease severity in a murine model of CNS autoimmunity, and express increased astrocyte-specific IRF1 and Caspase-1, suggesting an amplified interferon response in vivo. Additionally, we demonstrate that BATF2 is expressed primarily in astrocytes within multiple sclerosis lesions and that this expression is co-localized with IRF1. Collectively, our results further support evidence of protective functions for IFNg and implicate BATF2 as a key suppressor of overactive immune signaling in astrocytes during neuroinflammation.

2025-01-30 | GSE288440 | GEO

The transcriptome of type I murine astrocytes under interferon-gamma exposure and remyelination stimulus

Project description:Astrocytes are considered as an important contributor of the central nervous system (CNS) disorders, and particularly multiple sclerosis. Transcriptome of these cells is greatly affected by cytokines released by lymphocytes penetrating the blood-brain barrier, particularly classical pro-inflammatory cytokine interferon-gamma (IFN-gamma). We report here transcriptomal profiling of astrocytes treated by IFN-gamma and perspective remyelinization agent benztropine. Our findings indicate that expression of genes involved in antigen processing and presentation in astrocytes are significantly upregulated upon IFN-gamma exposure emphasizing critical role of this cytokine in redirecting of immune response towards self-antigens. Data reported herein support previous observations that IFN-gamma-induced JAK-STAT signaling pathway may be regarded as valuable target for the pharmaceutical intervention.

2017-03-23 | GSE96899 | GEO

Analysis of astrocyte interferon gamma signaling during EAE.

Project description:We identify pathways regulated by interferon gamma in astrocytes during EAE

2021-01-09 | GSE144872 | GEO

Proteomic profiling of interferon-responsive reactive astrocytes in rodent and human

Project description:Astrocytes are a heterogenous population of glial cells that respond to pathological insults or injury by undergoing a profound transformation called reactivity. Reactive astrocytes exhibit distinct, context-dependent cellular, molecular, and functional states that can either help or hinder tissue homeostasis. We recently identified a subtype of reactive astrocytes in the mouse brain called interferon-responsive reactive astrocytes (IRRAs), defined by interferon-responsive genes like Igtp, Ifit3, Oasl, Mx1, Cxcl10, and Gbp2 . To further this transcriptomic definition of IRRAs, we wanted to define the proteomic changes that occur in this sub-state.

2023-03-07 | MSV000091426 | MassIVE

RNA-seq of monocyte derived macrophages exposed to arachidonic acid, interferon beta, or interferon gamma

Project description:Monocyte derived macrophages were exposed to arachidonic acid, interferon beta, or interferon gamma

2021-12-31 | E-MTAB-10867 | biostudies-arrayexpress

Conserved interferon-gamma signaling and decreased immune exclusion programs in responses to immune checkpoint blockade therapy

Project description:We analyzed baseline and on-therapy tumor biopsies from 101 patients with advanced melanoma treated with nivolumab (anti-PD-1) alone or combined with ipilimumab (anti-CTLA-4). Analysis of whole transcriptome data showed that T cell infiltration and interferon-gamma signaling signatures corresponded most highly with clinical response to therapy, with a reciprocal decrease in cell cycle and WNT signaling pathways in responding biopsies. Clinical outcome differences were likely not due to differential melanoma cell responses to interferon-gamma, as 57 human melanoma cell lines exposed in vitro to this cytokine showed a conserved interferon-gamma transcriptome response unless they had mutations that precluded signaling from the interferon-gamma receptor. Therefore, the magnitude of the antitumor T cell response and the corresponding downstream interferon-gamma signaling are the main drivers of clinical response or resistance to immune checkpoint blockade therapy.

| EGAS00001004545 | EGA

Manx Shearwater Interferon gamma gene

Project description:sequencing of the Manx Shearwater Interferon gamma gene

| PRJEB20061 | ENA

Transcription profiling of Toxoplasma-infected human fibroblasts treated with human recombinant interferon gamma

Project description:Human fibroblasts were infected or not with Toxoplasma gondii (Pru strain) for 18 h at a nominal MOI of 3. Cells were subsequently treated with human recombinant interferon gamma (0.5 ng/ml = 30 pM) for 0, 2, 4 and 8 h before RNA was harvested for cDNA microarray experiments. Uninfected samples were named N0, N2, N4 and N8 (i.e., N2 indicated uninfected cells treated with interferon gamma for 2 h); infected samples were named P0, P2, P4 and P8. Duplicate cultures were analyzed for each condition (indicated as "a" and "b"). The reference channel (ch1, green) contained Universal Human Reference RNA. Using a genome-wide microarray analysis we show here a complete dysregulation of interferon-gamma-inducible gene expression in human fibroblasts infected with Toxoplasma. Notably, 46 of the 127 interferon-gamma-responsive genes were induced and 19 were suppressed in infected cells before they were exposed to interferon gamma, indicating that other stimuli produced during infection may also regulate these genes. Following interferon-gamma treatment, none of the 127 interferon-gamma-responsive genes could be significantly induced in infected cells.

2007-06-06 | E-SMDB-3827 | biostudies-arrayexpress

Expression data from HeLa cells upon interferon-gamma or interferon-beta treatment

Project description:Immune interferon beta and gamma are essential for mammalian host defence against intracellular pathogens. We used microarrays to detail the global programme of gene expression upon interferon-gamma or interferon-beta treatment and identified distinct classes of up-regulated genes.

2017-09-02 | GSE103363 | GEO

Autism-associated CHD8 controls reactive gliosis and neuroinflammation via remodeling chromatin in astrocytes [ATAC-seq]

Project description:Reactive changes of glial cells during neuroinflammation impact brain disorders and disease progression. Elucidating the mechanisms that control reactive gliosis may help understand brain pathophysiology and improve outcomes. Here, we report that adult ablation of the ASD-associated CHD8 in astrocytes attenuates reactive gliosis via remodeling chromatin accessibility, changing gene expression. Conditional Chd8 deletion in astrocytes, but not microglia, suppresses reactive gliosis by impeding astrocyte proliferation and morphological elaboration. Astrocyte Chd8 ablation alleviates lipopolysaccharide-induced neuroinflammation and septic-associated hypothermia in mice. Astrocytic CHD8 plays an important role in neuroinflammation by altering the chromatin landscape, regulating metabolic and lipid-associated pathways, and astrocyte-microglia crosstalk. Moreover, we show that reactive gliosis can be directly mitigated in vivo using an AAV-mediated Chd8 gene editing strategy. These findings uncover a role of ASD-associated CHD8 in the adult brain, which may warrant future exploration of targeting epigenetic pathways in reactive gliosis and neuroinflammation in injury and neurological diseases.

2024-07-09 | GSE271652 | GEO

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