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Divergent principles specifying inflammatory versus antiviral transcriptional programs in dendritic cells [ChIP-seq]

ABSTRACT: Stimulus-specific gene expression programs are enabled by enhancers, on which stimulus-regulated transcription factors (SRTFs) can land in a cell type- and stimulus-dependent manner. In this study, we identified the key features of enhancers that mediate differential responses to Toll-like receptor (TLR)-stimulation. We characterized the TLR3- and TLR9-induced programs and enhancers in CD8+ dendritic cells.The relevance of these features has been confirmed via machine learning application and by mapping SRTF-binding.

ORGANISM(S): Mus musculus

PROVIDER: GSE106730 | GEO | 2019/07/31

REPOSITORIES: GEO

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Divergent principles specifying inflammatory versus antiviral transcriptional programs in dendritic cells [ATAC-seq]

Project description:Stimulus-specific gene expression programs are enabled by enhancers, on which stimulus-regulated transcription factors (SRTFs) can land in a cell type- and stimulus-dependent manner. In this study, we identified the key features of enhancers that mediate differential responses to Toll-like receptor (TLR)-stimulation. We characterized the TLR3- and TLR9-induced programs and enhancers in CD8+ dendritic cells.The relevance of these features has been confirmed via machine learning application and by mapping SRTF-binding.

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Project description:TLR3, TLR7, and TLR9 stimulation induces many mouse inflammatory and autoimmune cytokines or immune receptors

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TLR3, TLR7, and TLR9 stimulation in murine dorsal root ganglion neurons

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Specificity of enhancer selection by IRF3, IRF5 and IRF9 in dendritic cells

Project description:To discover the key determinants of IRF-specific enhancer selection, we identified and characterized IRF binding regions. Using chromatin immunoprecipitation coupled with deep sequencing (ChIP-seq), we mapped the binding regions of IRF3, IRF5, and IRF9 in murine dendritic cells (DCs) stimulated with TLR3 and TLR9 agonists, as well as IFNβ, respectively. We comprehensively analysed the IRF cistromes to identify characteristic features, including DNA motifs for IRFs and other transcription factors, and chromatin status.

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Latent enhancers unveiled by stimulation expand and adapt the available cis-regulatory repertoire (FAIRE-seq)

Project description:According to current models, transcription factors (TFs) activated by extracellular stimuli operate in the context of a pre-established enhancer repertoire induced and maintained by lineage-specific TFs. Here, we uncovered the existence of latent enhancers, defined as regions of the genome that in terminally differentiated cells are poorly accessible and lack the histone marks characteristic of enhancers, but readily acquire these features in response to extracellular cues. Stimulation of resting macrophages caused simultaneous binding of stimulus-activated TFs and lineage-determining TFs to these regions, enabling deposition of enhancer-specific features. Once unveiled, these enhancers did not return to a latent state even when stimulation ceased; instead, they persisted and mediated a faster and stronger response upon restimulation. We suggest that stimulus-specific expansion of the available cis-regulatory repertoire provides an epigenomic memory of the exposure to environmental agents. Formaldehyde-Assisted Isolation Of Regulatory Elements (FAIRE) followed by multiparallel sequencing was performed in untreated murine bone marrow-derived macrophages.

2013-01-17 | E-GEOD-41677 | biostudies-arrayexpress

Mus musculus

Project description:Differential responses to TLR3 and TLR9 activation in Dendritic Cells

| PRJNA338146 | ENA

Divergent principles specifying inflammatory versus antiviral transcriptional programs in dendritic cells

Project description:Divergent principles specifying inflammatory versus antiviral transcriptional programs in dendritic cells

| PRJNA417853 | ENA

miRNA profiles in unstimulated and TLR stimulated MDMs

Project description:Macrophages play a crucial role in HIV-1 pathogenesis. Toll-like receptors (TLRs) are fundamental for innate and adaptive immune responses, but their role in HIV-1 infection is still incompletely understood. The TLR3 and TLR4 ligands poly(I:C) and LPS are known to modulate HIV-1 infection of and replication in monocyte-derived macrophages (MDMs), but the mechanism is incompletely understood. We found that MDMs stimulation with poly(I:C) or LPS abrogated infection by CCR5-using, macrophage-tropic HIV-1, or by VSV-G-pseudotyped HIV-1 virions, while TLR7 and TLR9 agonists Imiquimod and CpG only reduced infection to varying extent. Suppression of infection, or lack thereof, did not correlate with differential effects on CD4 or CCR5 expression, type I interferon induction, or production of pro-inflammatory cytokines. Furthermore, integrated pro-viruses were readily detected in unstimulated, TLR7- and TLR9-stimulated cells, but not in TLR3- or TLR4-stimulated MDMs, suggesting the alteration of post-entry, pre-integration event(s). MicroRNA (miRNA) microarray and real time PCR demonstrated increased miR-155 levels in MDMs upon TLR3/4, but not TLR7, stimulation, and a miR-155 inhibitor partially restored infectivity in poly(I:C)-stimulated MDMs. Finally, miR-155 over-expression in MDMs and cell lines remarkably diminished HIV-1 infection, inducing an accumulation of late reverse transcription products, concurrently with a decrease in mRNA levels of several HIV-1 dependency factors involved in nuclear import of pre-integration complexes. Our results suggest that miR-155 may target mRNA(s) for host cell protein(s) that either participate in or facilitate post-entry, pre-integration events, resulting in severely diminished HIV-1 infection. miRNA profiles were investigated in total RNA isolated from unstimulated and TLR3-, TLR4- and TLR7-stimulated human MDMs from a single normal donor

2011-12-14 | E-GEOD-34428 | biostudies-arrayexpress

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