Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Sustained R848 treatment of Mice

ABSTRACT: PCR Array Profiling - R848 does not induce TLR-signaling related genes in TLR7-/- mice. Aim: To corroborate TLR7-dependency of R848 in mice "Triggering TLR7 in mice induces immune activation and lymphoid system disruption, resembling HIV-mediated pathology", Baenziger et al. Blood 2008

ORGANISM(S): Mus musculus

PROVIDER: GSE12957 | GEO | 2008/09/30

SECONDARY ACCESSION(S): PRJNA110941

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Microarray analyses using bone marrow-derived macrophages from Batf2−/− and wildtype mice that had been stimulated with R848

Project description:We assessed the role of basic leucine zipper transcription factor ATF-like 2 (Batf2), particularly its positive transcriptional activities via TLR signals. Because TLR7 agonists are clinically used against tumors and have proven effective as antitumor drugs, we assessed effect of Batf2 on the responses to the TLR7 ligand (R848).

2017-07-24 | GSE101781 | GEO

Microarry datasets for RAW cells stimulated with R848 in the absence or presence of apilimod or API09

Project description:Apilimod is a reported TLR pathway antagonist in clinical trial. To understand the mode of action of apilimod, we applied global microarray analysis to explore the effect of apilimod on gene expression of RAW cell in the absence of presence of R848 (TLR7 ligand). RAW cells were stimulated with R848 in the absence or presence of apilimod (1μM). mRNAs were extracted at 0h, 1h,3h, 7h, and 22h for affymetrix analysis. The inactive analog of apilimod (API09) was included as a control.

2014-02-18 | E-GEOD-22124 | biostudies-arrayexpress

Microarry datasets for RAW cells stimulated with R848 in the absence or presence of apilimod or API09

2014-02-18 | GSE22124 | GEO

TLR signalling induced by bacterial RNA vs R848

Project description:Murine dendritic cells were derived from bone-marrow of 4 mice using GM-CSF. The DC were treated with RNA from gram-positive bacteria Listeria monocytogenes packaged in DOTAP or TLR7 agonist R848. Negative controls were DOTAP with no RNA or mock.

2012-05-08 | E-MTAB-1139 | biostudies-arrayexpress

mouse BMDM poly(I:C), R848, or poly(I:C)+R848 stimulation

Project description:Gene expression kinetics for BM-DM from C57BL/6 mice challenged by poly(I:C) , R848, poly(I:C)+R848 examined at 6 time points including 0.5, 1, 2, 4, 8, 12 h.

2017-08-17 | GSE89987 | GEO

mouse BMDM dual PAMP stimulation with poly(I:C), R848, LPS, Pam3CSK3

Project description:Gene expression kinetics for BM-DM from C57BL/6 mouse stimulated with four different TLR ligands poly(I:C), R848, LPS, Pam3CSK4 either singly or in paired combination, for 1 hour, 4 hour, or 8 hour.

2017-08-17 | GSE89962 | GEO

TLR signaling in C57BL/6J TLR7-tolerant CD3+ T-cells over B6 TLR7 null CD3+ T-cells.

Project description:Murine CD3+ T-cells were immunomagnetically purified from the spleens of C57BL/6J mice and were pretreated in vitro for three days in the presence of R848 (5 μg/ml). Gene expression profile of wild type (WT) C57BL/6J TLR7-primed T-cells, was compared to unmanipulated B6 TLR7 null CD3+ Τ-cells. We used Qiagen Toll-like Receptor RT2 Profiler PCR Array kit to quantitate gene expression profiling of the TLR signaling pathway.

2017-04-21 | GSE80573 | GEO

Single cell mRNA sequencing of Peyer's patch CD11c+ phagocytes from unstimulated or R848- or CpG-stimulated mice

Project description:We deciphered the transcriptional landscape of Peyer's patch CD11c+ phagocytes from their emergence in the tissue to their final maturation state at homeostasis and under stimulation with the TLR7 ligand R848 and the TLR9 ligand CpG.

2023-05-04 | GSE221315 | GEO

Dysregulated TLR7 signaling drives anemia via development of hemophagocytic macrophages

Project description:The debilitating autoimmune disease Systemic Lupus Erythematosus (SLE) is closely associated with Toll-like receptor (TLR) 7 and type I interferon (IFN) activity in humans and in murine SLE-like disease. Two central manifestations of SLE affect the myeloid lineage of the immune system, myeloid expansion and anemia. Yet, whether these symptoms are linked and the role of TLR7 and/or type I IFN in these processes is unclear. Here we show that TLR7 signaling promotes cell-autonomous, phosphoinositide 3-kinase (PI3K)- and mammalian target of rapamycin (mTOR)-dependent macrophage development from the common myeloid progenitor (CMP). Strikingly, this TLR7-driven macrophage development requires and is enhanced by type I IFN. Genome-wide transcriptional profiling and functional studies demonstrated that TLR7 promoted the expression of Spic, the master regulator of splenic red pulp macrophages (RPM) and preferential development of hemophagocytic RPM-like cells from CMP in vitro. We found increased incidence of RPM-like cells in vivo in a mouse model of SLE caused by TLR7 overexpression, which correlated with decreased red blood cell (RBC) count and anemia. These findings demonstrate a mechanism by which TLR7 signaling promotes anemia that is of clinical significance in SLE, other rheumatological diseases and chronic viral infections. This work also identifies a previously unknown molecular pathway by which TLR signaling and type I IFN synergize to promote myeloid development from hematopoietic progenitors. CMP were sorted from the bone marrow of wild-type C57BL/6 mice, cultured with SCF+R848 or SCFr+MCSF, and CD11b+F4/80+ macrophages sorted after 5 days, n=3 per group

2016-07-01 | E-GEOD-70520 | biostudies-arrayexpress

Transcription profiling of human dendritic cells to identify a combinatorial code by which DCs discriminate pathogens and provide (suggest) a rationale to design adjuvants for TH1 responses.

Project description:Toll like receptors (TLRs) sense microbial products and initiate adaptive immune responses by activating dendritic cells (DCs). Since pathogens may contain several agonists we asked whether different TLRs may synergize in DC activation. We report that in human and mouse DC TLR3 or TLR4 potently synergize with TLR7, TLR8 or TLR9 in the induction of selected cytokine genes. Upon synergistic stimulation, IL-12, IL-23 and Delta-4 are induced at levels 50-100 fold higher than those induced by optimal concentrations of single agonists, leading to enhanced and sustained TH1 polarizing capacity. Using microarray analysis we show that only 1.5% of the transcripts induced by single TLR agonists are synergistically regulated by combinations of TLR4 and TLR8 agonists.. These results identify a combinatorial code by which DCs discriminate pathogens and provide (suggest) a rationale to design adjuvants for TH1 responses. Series_overall_design: 3 untreated, 3 treated with LPS at 2h, 3 treated with LPS at 8h, 3 treated with R848 at 2h, 3 treated with R848 at 8h, 3 treated with LPS + R848 at 2h, 3 treated with LPS + R848 at 8h

2007-09-14 | E-GEOD-2706 | biostudies-arrayexpress

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