Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

IRF5 regulates unique subset of genes in mouse dendritic cells during West Nile virus infection

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE114993 | GEO | 2018/12/14

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

IRF5 regulates unique subset of genes in dendritic cells during West Nile virus infection.

Project description:Pathogen recognition receptor (PRR) signaling is critical for triggering innate immune activation and the expression of immune response genes, including genes that impart restriction against virus replication. RIG-I-like receptors and TLRs are PRRs that signal immune activation and drive the expression of antiviral genes and the production of type I IFN leading to induction of IFN-stimulated genes, in part through the interferon regulatory factor (IRF) family of transcription factors. Previous studies with West Nile virus (WNV) showed that IRF3 and IRF7 regulate IFN expression in fibroblasts and neurons, whereas macrophages and dendritic cells (DCs) retained the ability to induce IFN-? in the absence of IRF3 and IRF7 in a manner implicating IRF5 in PRR signaling actions. Here we assessed the contribution of IRF5 to immune gene induction in response to WNV infection in DCs. We examined IRF5-dependent gene expression and found that loss of IRF5 in mice resulted in modest and subtle changes in the expression of WNV-regulated genes. Anti-IRF5 chromatin immunoprecipitation with next-generation sequencing of genomic DNA coupled with mRNA analysis revealed unique IRF5 binding motifs within the mouse genome that are distinct from the canonical IRF binding motif and that link with IRF5-target gene expression. Using integrative bioinformatics analyses, we identified new IRF5 primary target genes in DCs in response to virus infection. This study provides novel insights into the distinct and unique innate immune and immune gene regulatory program directed by IRF5.

| S-EPMC6355374 | biostudies-literature

IRF5 regulates unique subset of genes in mouse dendritic cells during West Nile virus infection (RNA-Seq)

Project description:Using integrative bioinformatics analyses, we identified new IRF5 primary target genes in mouse DCs in response to virus infection. This study provides novel insights into the distinct and unique innate immune and immune gene regulatory program directed by IRF5.

2018-12-14 | GSE114992 | GEO

IRF5 regulates unique subset of genes in mouse dendritic cells during West Nile virus infection (ChIP-Seq)

2018-12-14 | GSE114991 | GEO

IRF5 regulates unique subset of genes in mouse dendritic cells during West Nile virus infection (BMM_RNA-Seq)

2018-12-14 | GSE118452 | GEO

IRF5 regulates unique subset of genes in mouse dendritic cells during West Nile virus infection

Project description:IRF5 regulates unique subset of genes in mouse dendritic cells during West Nile virus infection

| PRJNA473488 | ENA

IRF5 regulates unique subset of genes in mouse dendritic cells during West Nile virus infection (BMM_RNA-Seq)

Project description:IRF5 regulates unique subset of genes in mouse dendritic cells during West Nile virus infection (BMM_RNA-Seq)

| PRJNA485698 | ENA

IRF5 regulates unique subset of genes in mouse dendritic cells during West Nile virus infection (ChIP-Seq)

Project description:IRF5 regulates unique subset of genes in mouse dendritic cells during West Nile virus infection (ChIP-Seq)

| PRJNA473491 | ENA

IRF5 regulates unique subset of genes in mouse dendritic cells during West Nile virus infection (RNA-Seq)

Project description:IRF5 regulates unique subset of genes in mouse dendritic cells during West Nile virus infection (RNA-Seq)

| PRJNA473490 | ENA

West Nile virus infection of human monocyte-derived dendritic cells

Project description:West Nile virus (WNV) is a neurotropic flavivirus and the leading cause of mosquito-borne encephalitis in the United States. Recent studies in humans have found that dysfunctional T cell responses strongly correlate with development of severe WNV neuroinvasive disease. However, the contributions of human dendritic cells (DCs) in priming WNV-specific T cell immunity remains poorly understood. Here, we demonstrate that human monocyte derived DCs (moDCs) support productive viral replication following infection with a pathogenic strain of WNV. Antiviral effector gene transcription was strongly induced during the log-phase viral growth, while secretion of type I interferons (IFN) occurred with delayed kinetics. Activation of RIG-I like receptor (RLR) or type I IFN signaling prior to log-phase viral growth significantly diminished viral replication, suggesting that early activation of antiviral programs can block WNV infection. In contrast to the induction of antiviral responses, WNV infection did not promote transcription or secretion of pro-inflammatory (IL-6, GM-CSF, CCL3, CCL5, CXCL9) or T cell modulatory cytokines (IL-4, IL-12, IL-15). There was also minimal induction of molecules associated with antigen presentation and T cell priming, including the co-stimulatory molecules CD80, CD86, and CD40. Functionally, WNV-infected moDCs dampened allogenic CD4 and CD8 T cell activation and proliferation. Combined, we propose a model where WNV subverts human DC activation to compromise priming of WNV-specific T cell immunity.

2019-09-06 | GSE136342 | GEO

gammadelta T cells promote the maturation of dendritic cells during West Nile virus infection.

Project description:gammadelta T cells are important for the early control of West Nile virus (WNV) dissemination. Here, we investigated the role of gammadelta T cells in the regulation of CD4(+) T-cell response following a WNV challenge. Splenic dendritic cells (DCs) of WNV-infected gammadelta T-cell-deficient (TCRdelta(-/-)) mice displayed lower levels of CD40, CD80, CD86 and major histocompatibility complex (MHC) class II expression and interleukin-12 (IL-12) production than those of wild-type mice. Naïve DCs cocultured with WNV-infected gammadelta T cells showed enhanced levels of costimulatory molecules, MHC class II expression and IL-12 production. Further, coculture of CD4(+) T cells from OT II transgenic mice with DCs of WNV-infected TCRdelta(-/-) mice induced less interferon-gamma (IFN-gamma) and IL-2 production than with those of wild-type controls. Viral antigens were detected in WNV-infected gammadelta T cells.WNV infection or toll-like receptor (TLR) agonist treatment of gammadelta T cells induced the production of IFN-gamma, tumor necrosis factor-alpha and IL-6, which are known to promote DC maturation. Nevertheless, the levels of TLRs 2, 3, 4 and 7 expression of WNV-infected gammadelta T cells were not different from those of noninfected cells. Overall, these data suggest that WNV-induced gammadelta T-cell activation promotes DC maturation and initiates CD4(+) T-cell priming.

| S-EPMC2954433 | biostudies-literature

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