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Monocyte-derived macrophages stimulated with the TLR8 agonist 3M-002 at 10 microM show a prominent activation of TLR-dependent genes as assessed b "Human Toll-like Receptor PCR array pathway" over time

ABSTRACT: We were interested in the effects of TLR8 triggering of human monocyte-derived macrophages. We observed a striking upregulation of those genes. This work was done in the context of examining the effects of TLR8 triggering for the activation of HIV.

ORGANISM(S): Homo sapiens

PROVIDER: GSE26470 | GEO | 2011/01/11

SECONDARY ACCESSION(S): PRJNA136543

REPOSITORIES: GEO

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Monocyte-derived macrophages stimulated with the TLR8 agonist 3M-002 at 10 microM show a prominent activation of TLR-dependent genes as assessed b "Human Toll-like Receptor PCR array pathway" over time

Project description:We were interested in the effects of TLR8 triggering of human monocyte-derived macrophages. We observed a striking upregulation of those genes. This work was done in the context of examining the effects of TLR8 triggering for the activation of HIV. We generated monocyte-derived macrophages (MDM) by initially isolating monocytes and subsequently culturing them in RPMI supplemented with human AB serum. MDM were stimulated for 18 h with the TLR8 agonist 3M-002, and subsequently harvested for extraction of total RNA. Total RNA was then used to quantify the TLR-dependent genes using a PCR array pathway.

2011-01-11 | E-GEOD-26470 | biostudies-arrayexpress

U1 cells stimulated with the TLR8 agonist 3M-002 at 10 microM show a prominent activation of TLR-dependent genes as assessed by "Human toll-like Receptor PCR array pathway" over time

2011-01-11 | GSE26469 | GEO

U1 cells stimulated with the TLR8 agonist 3M-002 at 10 microM show a prominent activation of TLR-dependent genes as assessed by "Human toll-like Receptor PCR array pathway" over time

Project description:We investigated the effects of the TLR8 agonist 3M-002 on latently HIV infected U1 cells. We found a prominent upregulation of TLR-dependent genes. Notably, the TLR8 agonist resulted in a marked activation of HIV. We stimulated U1 cells for 6 or 10 hours with 3M-002 and subsequently harvested the cells, extracted total RNA. RNA was then used for quantifiying TLR-dependent gene upregulation using a commercial PCR array pathway

2011-01-11 | E-GEOD-26469 | biostudies-arrayexpress

Treatment of human monocytes with TLR7 or TLR8 agonists

Project description:Goal was to detect differences in response to TLR7 versus TLR8 agonists in human monocytes from healthy donors 3 deidentified donors from the Red Cross, monocytes from each donor incubated overnight with either vehicle, TLR7 agonist or TLR8 agonist

2014-12-24 | E-GEOD-64480 | biostudies-arrayexpress

Bacterial RNA sensing by TLR8 requires RNase 6 processing and is inhibited by RNA 2’O-methylation

Project description:Mechanistic studies have revealed that TLR8 senses single-stranded RNA (ssRNA) fragments, processed via synergistic cleavage by ribonucleases (RNase) T2 and RNase A family members. Processing by these RNases releases uridines and purine-terminated residues resulting in TLR8 activation. Monocytes show high expression of RNase 6, yet this RNase has not been analyzed for its physiological contribution to recognition of bacterial RNA by TLR8. Herein, we characterized molecular RNase 6 cleavage mechanisms. BLaER1 RNASE6-/- cells showed a dampened TLR8-dependent response upon stimulation with isolated bacterial RNA (bRNA) but also upon infection with live whole bacteria. Pretreatment of bacterial RNA with recombinant RNase 6 generated fragments that induced stimulation in RNASE6 knockout cells. 2’O-RNA methyl modification, when introduced at the first uridine in the UA dinucleotide, impaired upstream processing by RNase 6 and dampened TLR8 stimulation. In summary, this data shows that RNase 6 plays a critical role in the processing of bacterial RNA by generating uridine-terminated breakdown products that ultimately activate TLR8.

2024-09-12 | PXD053881 | Pride

STING is essential for TLR8 induced IFN

Project description:The innate immune system is equipped with multiple receptors to detect microbial nucleic acids and induce type I interferon (IFN) to restrict viral replication. When dysregulated these receptor pathways induce inflammation in response to host nucleic acids and promote development and persistence of autoimmune diseases like Systemic Lupus Erythematosus (SLE). IFN production is regulated by the Interferon Regulatory Factor (IRF) transcription factor family of proteins that function downstream of several innate immune receptors such as Toll-like receptors (TLRs) and Stimulator of Interferon Genes (STING). Although both TLRs and STING activate the same downstream molecules, the pathway by which TLRs and STING activate IFN response are thought to be independent. Here we show that STING plays a previously undescribed role in human TLR8 signaling. Stimulation with the TLR8 ligands induced IFN secretion in primary human monocytes, and inhibition of STING reduced IFN secretion from primary monocytes from 8 healthy donors. We demonstrate that TLR8-induced IRF activity was reduced by STING inhibitors. Moreover, TLR8-induced IRF activity was blocked by inhibition or loss of IKKε, but not TBK1. Bulk RNA transcriptomic analysis supported a model where TLR8 induces transcriptional responses associated with SLE that can be downregulated by inhibition of STING. These data demonstrate that STING is required for full TLR8-to-IRF signaling and provide evidence for a new framework of crosstalk between cytosolic and endosomal innate immune receptors, which could be leveraged to treat IFN driven autoimmune diseases.

2024-06-03 | GSE233450 | GEO

Phagosomal signaling by Borrelia burgdorferi in human monocytes involves Toll-like receptor (TLR) 2 and TLR8 cooperativity and TLR8-mediated induction of IFN-beta.

Project description:Phagocytosed Borrelia burgdorferi (Bb) induces inflammatory signals that differ both quantitatively and qualitatively from those generated by spirochetal lipoproteins interacting with Toll-like receptor (TLR) 1/2 on the surface of human monocytes. Of particular significance, and in contrast to lipoproteins, internalized spirochetes induce transcription of IFN-?. Using inhibitory immunoregulatory DNA sequences (IRSs) specific to TLR7, TLR8, and TLR9, we show that the TLR8 inhibitor IRS957 significantly diminishes production of TNF-?, IL-6, and IL-10 and completely abrogates transcription of IFN-? in Bb-stimulated monocytes. We demonstrate that live Bb induces transcription of TLR2 and TLR8, whereas IRS957 interferes with their transcriptional regulation. Using confocal and epifluorescence microscopy, we show that baseline TLR expression in unstimulated monocytes is greater for TLR2 than for TLR8, whereas expression of both TLRs increases significantly upon stimulation with live spirochetes. By confocal microscopy, we show that TLR2 colocalization with Bb coincides with binding, uptake, and formation of the phagosomal vacuole, whereas recruitment of both TLR2 and TLR8 overlaps with degradation of the spirochete. We provide evidence that IFN regulatory factor (IRF) 7 is translocated into the nucleus of Bb-infected monocytes, suggesting its activation through phosphorylation. Taken together, these findings indicate that the phagosome is an efficient platform for the recognition of diverse ligands; in the case of Bb, phagosomal signaling involves a cooperative interaction between TLR2 and TLR8 in pro- and antiinflammatory cytokine responses, whereas TLR8 is solely responsible for IRF7-mediated induction of IFN-?.

| S-EPMC3048123 | biostudies-literature

Reversal of human regulatory T cell suppression throgh TLR8 signaling

Project description:Analyses of gene alterations of human Treg cells treated with or without TLR8 ligand using the Illumina whole-genome Human HT-12 BeadChips. The study will provide important information for the molecular signature changes during the reversal of human Treg suppression mediated by activation of TLR8 signaling.

2018-12-30 | GSE118311 | GEO

Treatment of human monocytes with TLR7 or TLR8 agonists

Project description:Goal was to detect differences in response to TLR7 versus TLR8 agonists in human monocytes from healthy donors

2014-12-24 | GSE64480 | GEO

Quantitative Analysis of CXCL4 and TLR8 signaling crosstalk in human primary monocytes by RNA-Seq

Project description:To gain a comprehensive understanding of gene regulation in CXCL4 and TLR8 signaling crosstalk, we treated primary human blood monocytes with CXCL4 and TLR8 ssRNA ligand ORN8L for 6 h and performed transcriptomic analysis via RNA-seq. We observed that CXCL4 interacted with TLR8 ssRNA ligand and triggered inflammatory cytokine storm including IL6, IL12p40, TNF and IFNβ, and pro-fibrotic gene expression and activated NLRP3 inflammasome leading to interleukin-1β (IL-1β) secretion and pyroptosis in human blood monocytes.

2022-05-13 | GSE181889 | GEO

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