Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Chromatin accessibility profile of splenic LCMV-specific memory B cells following type I or II interferon blockade in acute versus chronic LCMV infection

ABSTRACT: Dynamics of interferon signalling impact the adaptive immune response. We used ATAC sequencing (ATAC-seq) to analyze chromatin accessibility in memory B cells from mice infected with acute or chronic LCMV infection, treated with type I or type II interferon blocking antibodies.

ORGANISM(S): Mus musculus

PROVIDER: GSE226485 | GEO | 2024/02/17

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Shared Molecules

Only show the datasets with similarity scores above: 0.5

Threshold

0.5

Similar Datasets

Chromatin accessibility profile of splenic LCMV-specific memory B cells following type I or II interferon blockade in acute versus chronic LCMV infection

Project description:Chromatin accessibility profile of splenic LCMV-specific memory B cells following type I or II interferon blockade in acute versus chronic LCMV infection

| PRJNA940424 | ENA

Chromatin accessibility profile at the single cell level of splenic LCMV-specific B cells in acute versus chronic LCMV infection [scATAC-seq]

Project description:Chronic viral infection disrupts memory B cell development. We used single cell ATAC sequencing (scATAC-seq) to analyze chromatin accessibility in antigen-specific B cells responding to acute versus chronic LCMV infection.

2024-02-17 | GSE225932 | GEO

Splenic LCMV-specific B cells in acute versus chronic LCMV infection

Project description:Splenic LCMV-specific B cells in acute versus chronic LCMV infection

| PRJNA947097 | ENA

Comparison of Trail+/+ versus Trail-/- splenic NK cells from naïve and LCMV-infected mice

Project description:Investigation of the change of the Trail-dependent NK cell transcriptome during short-term (24h) infection with lymphocytic choriomeningitis virus (LCMV). RNA sequencing-based transcriptomics analysis was performed in spleen-isolated (NK1.1+CD3-) NK cells from 3 naïve Trail+/+ mice, 3 naive Trail-/- mice, 4 LCMV-infected Trail+/+ mice, and 4 LCMV-infected Trail-/- mice.

2019-08-27 | E-MTAB-7562 | biostudies-arrayexpress

Gene expression profile at the single cell level of splenic LCMV-specific B cells in acute versus chronic LCMV infection [scRNA-seq, CITE-seq]

Project description:Chronic viral infection disrupts memory B cell development. We used single cell RNA sequencing (scRNA-seq) to analyze the diversity of antigen-specific B cells responding to acute versus chronic LCMV infection.

2024-02-17 | GSE225933 | GEO

ATAC-sequencing of Th1, Tfh, and memory-like splenic CD4+ T cells on day 14 post LCMV Cl13 infection

Project description:CD4+ T cell-derived interleukin 21 (IL-21) sustains CD8+ T cell responses during chronic viral infection, but the helper subset that confers this protection remains unclear. Here, we applied scRNA and ATAC-seq approaches to determine the heterogeneity of CD4+ T cells during LCMV clone 13 infection.

2022-02-25 | GSE193932 | GEO

Persistent LCMV infection is controlled by blockade of type I interferon signaling.

Project description:During persistent viral infections, chronic immune activation, negative immune regulator expression, an elevated interferon signature, and lymphoid tissue destruction correlate with disease progression. We demonstrated that blockade of type I interferon (IFN-I) signaling using an IFN-I receptor neutralizing antibody reduced immune system activation, decreased expression of negative immune regulatory molecules, and restored lymphoid architecture in mice persistently infected with lymphocytic choriomeningitis virus. IFN-I blockade before and after establishment of persistent virus infection resulted in enhanced virus clearance and was CD4 T cell-dependent. Hence, we demonstrate a direct causal link between IFN-I signaling, immune activation, negative immune regulator expression, lymphoid tissue disorganization, and virus persistence. Our results suggest that therapies targeting IFN-I may help control persistent virus infections.

| S-EPMC3640797 | biostudies-literature

Blockade of chronic type I interferon signaling to control persistent LCMV infection.

Project description:Type I interferons (IFN-I) are critical for antiviral immunity; however, chronic IFN-I signaling is associated with hyperimmune activation and disease progression in persistent infections. We demonstrated in mice that blockade of IFN-I signaling diminished chronic immune activation and immune suppression, restored lymphoid tissue architecture, and increased immune parameters associated with control of virus replication, ultimately facilitating clearance of the persistent infection. The accelerated control of persistent infection induced by blocking IFN-I signaling required CD4 T cells and was associated with enhanced IFN-γ production. Thus, we demonstrated that interfering with chronic IFN-I signaling during persistent infection redirects the immune environment to enable control of infection.

| S-EPMC3704950 | biostudies-literature

Single-cell RNA-sequencing of IL-21-tRFP+ GP66+ splenic CD4+ T cells on days 7 and 14 post LCMV Cl13 infection

2022-02-25 | GSE193935 | GEO

RNA sequencing of splenic reticular cells in healthy and LCMV-infected mice

Project description:We report the transcriptome of subsets of mouse splenic mesenchymal reticular cells and lymph node reticular cells obtained from healthy Ccl19-cre x R26R-EYFP mice on a C57BL/6 background. We also examine splenic reticular cells from these mice infected with lymphocytic choriomeningitis virus (LCMV) strain Armstrong (acute infection) or strain Clone 13 (chronic infection). Subsets of CD45- CD31- Ter119- reticular cells were analyzed including PDPN+ T zone reticular cells (TRC) and MAdCAM-1+ marginal reticular cells (MRC) from spleen and lymph nodes. Additionally from the spleen we analyzed PDPN+ CD140a- cells, PDPN+ EYFP- cells, and EYFP+ red pulp reticular cells (RPRC) in healthy mice. We analyzed TRC, MRC, PDPN+ EYFP- cells, and EYFP+ RPRC from mice infected with LCMV Armstrong or LCMV Clone-13 on day 8 or on day 30 after infection. Our study represents the first detailed analysis of splenic reticular cell transcriptomes in healthy and LCMV-infected mice, with biologic replicates, generated by RNA-sequencing. We find substantial differential gene expression across subsets of splenic and lymph node reticular cells. We reveal significant changes in gene expression induced after virus infection that differ markedly with disease.

2022-01-09 | GSE171124 | 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