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tlr7 8 ligand r848 (InvivoGen)

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Structured Review

InvivoGen tlr7 8 ligand r848

Genetic analysis of the proband. (A) De novo <t>TLR7</t> mutation identified by trio-based genome sequencing. (B) Conservation of the affected proline residue across species. (C and D) Location of P435S within the extracellular domain, relative to previously reported pathogenic variants (F507S/L, P267L, Y264H). (E) NF-κB reporter assay in HEK293T cells following <t>R848</t> stimulation. (F) Sustained type I interferon signaling in the TLR7-GOF patient compared to patients with monogenic type I interferonopathies. HC, healthy controls; SAVI, STING-associated vasculopathy with onset in infancy; TIR, Toll/interleukin-1 receptor/resistance protein; TM, transmembrane; ****P < 0.0001.

Tlr7 8 Ligand R848, supplied by InvivoGen, used in various techniques. Bioz Stars score: 99/100, based on 2404 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/tlr7+8+ligand/R848/pmc12991832-126-30-33
Average 99 stars, based on 2404 article reviews

tlr7 8 ligand r848 - by Bioz Stars, 2026-09

99/100 stars

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1) Product Images from "Novel TLR7 gain-of-function variant and review of the associated disease spectrum"

Article Title: Novel TLR7 gain-of-function variant and review of the associated disease spectrum

Journal: Journal of Human Immunity

doi: 10.70962/jhi.20250199

Genetic analysis of the proband. (A) De novo TLR7 mutation identified by trio-based genome sequencing. (B) Conservation of the affected proline residue across species. (C and D) Location of P435S within the extracellular domain, relative to previously reported pathogenic variants (F507S/L, P267L, Y264H). (E) NF-κB reporter assay in HEK293T cells following R848 stimulation. (F) Sustained type I interferon signaling in the TLR7-GOF patient compared to patients with monogenic type I interferonopathies. HC, healthy controls; SAVI, STING-associated vasculopathy with onset in infancy; TIR, Toll/interleukin-1 receptor/resistance protein; TM, transmembrane; ****P < 0.0001.

Figure Legend Snippet: Genetic analysis of the proband. (A) De novo TLR7 mutation identified by trio-based genome sequencing. (B) Conservation of the affected proline residue across species. (C and D) Location of P435S within the extracellular domain, relative to previously reported pathogenic variants (F507S/L, P267L, Y264H). (E) NF-κB reporter assay in HEK293T cells following R848 stimulation. (F) Sustained type I interferon signaling in the TLR7-GOF patient compared to patients with monogenic type I interferonopathies. HC, healthy controls; SAVI, STING-associated vasculopathy with onset in infancy; TIR, Toll/interleukin-1 receptor/resistance protein; TM, transmembrane; ****P < 0.0001.

Techniques Used: Mutagenesis, Sequencing, Residue, Reporter Assay

other:

Article Title: Substituted indazoles useful for treatment and prevention of allergic and/or inflammatory diseases in animals
Article Snippet: After this incubation time of 24 hours, the supernatants were harvested and analysed using a commercially available hIL-23 ELISA (eBiosciences, Cat. No. 88-7237-88), which was conducted according to the manufacturer's instructions.

Article Title: Use of 2-substituted indazoles for the treatment and prophylaxis of autoimmune diseases
Article Snippet: After incubation for 24 hours, the cell culture supernatants were removed and analysed by means of a commercially available human IFN-α ELISA (IFNalpha Multi-Subtype ELISA Kit, pbl Assay Science, Cat. No. 41105-1).

Article Title: CD24-Fc suppression of immune related adverse events in a therapeutic cancer vaccine model of murine neuroblastoma.
Article Snippet: TLR7/8 ligand (Resiquimod, R848) was purchased from InvivoGen (San Diego, California).

Article Title: CD24-Fc suppression of immune related adverse events in a therapeutic cancer vaccine model of murine neuroblastoma
Article Snippet: TLR7/8 ligand (Resiquimod, R848) was purchased from InvivoGen (San Diego, California).

Activation Assay:

Article Title: Substituted indazoles, methods for the production thereof, pharmaceutical preparations that contain said substituted indazoles, and use of said substituted indazoles to produce drugs
Article Snippet: The obtained pDCs were resuspended in complete medium (RPMI 1640+GlutaMax [Gibco, Cat. No. 61870-010] supplemented with 10% FBS [Gibco, Cat. No. 10493-106] and 50 U penicillin/streptomycin [Gibco, Cat. No. 15140-114]) and seeded at a cell density of 5×104 cells/well in a 96-well microtitre plate (Costar, Cat. No. 3599). .. The pDCs were stimulated either with a TLR7/8 ligand (imiquimod, R837, Invivogen, Cat. No. tlrl-imq) or with a TLR-9 ligand (CPG-A, ODN2216, Invivogen, Cat. No. tlrl-2216-1) and this led to activation of the IRAK4-mediated signalling pathways. .. After incubation for 24 hours, the cell culture supernatants were removed and analysed using a commercially available human IFNα ELISA (IFNalpha Multi-Subtype ELISA Kit, pbl Assay Science, Cat. No. 41105-1).

Article Title: Substituted indazoles, methods for the production thereof, pharmaceutical preparations that contain said new substituted indazoles, and use of said new substituted indazoles to produce drugs
Article Snippet: .. The pDCs were stimulated either with a TLR7/8 ligand (imiquimod, R837, Invivogen, Cat. No. tlrl-imq) or with a TLR-9 ligand (CPG-A, ODN2216, Invivogen, Cat. No. tlrl-2216-1) and this led to activation of the IRAK4-mediated signalling pathways. .. After incubation for 24 hours, the cell culture supernatants were removed and analysed using a commercially available human IFNα ELISA (IFNalpha Multi-Subtype ELISA Kit, pbl Assay Science, Cat. No. 41105-1).

Article Title: Substituted indazoles, methods for the production thereof, pharmaceutical preparations that contain said substituted indazoles, and use of said substituted indazoles to produce drugs
Article Snippet: After this incubation time of 24 hours, the supernatants were harvested and analysed using a commercially available hIL-23 ELISA (eBiosciences, Cat. No. 88-7237-88), which was conducted according to the manufacturer's instructions. .. The pDCs were stimulated either with a TLR7/8 ligand (imiquimod, R837, Invivogen, Cat. No. tlrl-imq) or with a TLR-9 ligand (CPG-A, ODN2216, Invivogen, Cat. No. tlrl-2216-1) and this led to activation of the IRAK4-mediated signalling pathways. .. After incubation for 24 hours, the cell culture supernatants were removed and analysed using a commercially available human IFNα ELISA (IFNalpha Multi-Subtype ELISA Kit, pbl Assay Science, Cat. No. 41105-1).

Sterility:

Article Title: Wound-Healing Potential of Engineered Lysin GRC-ML07 in Pseudomonas aeruginosa Infected Wounds in Immunocompromised Mice
Article Snippet: 6 , LPS (PC) , Purified lipopolysaccharide from E. coli strain 055:B5. TLR4 ligand (Charles River Laboratories). , Sterile. .. 7 , R848 (PC) , TLR7/8 ligand (Invivogen) , Sterile. ..

Image Search Results

a mRNA levels of Dpep2 in RAW264.7 cells were examined after stimulation with Pam3Csk4 (TLR1/2 ligand), LPS (TLR4 ligand), R848 (TLR7/8 ligand) and poly (I:C) (TLR3 ligand) for 12 h ( n = 3 biological replicates). b , c mRNA expressions of DPEP2 in human monocytes ( b ) or bone marrow-derived macrophages (BMDM) ( c ) were examined after LPS stimulation for 12 h with different doses ( n = 3 biological replicates). d mRNA expressions of Dpep2 in RAW264.7 cells were examined after LPS stimulation for 6 or 12 h with different doses ( n = 3 biological replicates). e Protein levels of DPEP2 in RAW264.7 cells were examined after LPS stimulation for 24 h with different doses ( n = 3 biological replicates). f – g RAW264.7 cells with Dpep2 deficiency (sh Dpep2 RAW264.7 cells, n = 4 biological replicates) and control RAW264.7 cells (shNT RAW264.7 cells, n = 3 biological replicates) were obtained for RNA-seq analysis; f Volcano plot showing results from differential expression analysis. Genes with P-adjusted value < 0.05 are highlighted in red or blue; g Bar plot showing the GSEA results in sh Dpep2 vs shNT RAW264.7 cells. h – k Levels of interleukin (IL)-1β, IL-6 and tumor necrosis factor-α (TNF) in sh Dpep2 vs shNT BMDMs and Dpep2 knockout ( Dpep2 KO) vs wild type (WT) mice derived BMDMs were analyzed ( n = 3 biological replicates). l, m IL-1β, IL-6 and TNF secretion of sh Dpep2 vs shNT RAW264.7 cells and Dpep2 KO vs WT mice derived BMDMs were analyzed at 24 h after LPS stimulation ( n = 3 biological replicates). n - o RAW264.7 cells and BMDMs overexpressing Dpep2 (DPEP2) and relatively control vector (Vector) cells were constructed. Levels of IL-1β, IL-6, and TNF secreted by DPEP2 cells vs Vector cells were analyzed at 24 h after LPS stimulation ( n = 3 biological replicates). Data represent the mean ± standard deviation. ns, not significant. One-way ANOVA followed by the Bonferroni multiple comparisons was used in ( a – c, e ), two-way repeated measures ANOVA with Tukey’s multiple comparisons test was used in ( d ), two-sided Wilcoxon rank-sum test was used in ( f ) and two-sided unpaired Student’s t test was used in ( h–o ). NES, n o rmalized enrichment score.

Journal: Nature Communications

Article Title: DPEP2 suppresses hyperinflammation via metabolic reprogramming of macrophages in sepsis

doi: 10.1038/s41467-026-70466-4

Figure Lengend Snippet: a mRNA levels of Dpep2 in RAW264.7 cells were examined after stimulation with Pam3Csk4 (TLR1/2 ligand), LPS (TLR4 ligand), R848 (TLR7/8 ligand) and poly (I:C) (TLR3 ligand) for 12 h ( n = 3 biological replicates). b , c mRNA expressions of DPEP2 in human monocytes ( b ) or bone marrow-derived macrophages (BMDM) ( c ) were examined after LPS stimulation for 12 h with different doses ( n = 3 biological replicates). d mRNA expressions of Dpep2 in RAW264.7 cells were examined after LPS stimulation for 6 or 12 h with different doses ( n = 3 biological replicates). e Protein levels of DPEP2 in RAW264.7 cells were examined after LPS stimulation for 24 h with different doses ( n = 3 biological replicates). f – g RAW264.7 cells with Dpep2 deficiency (sh Dpep2 RAW264.7 cells, n = 4 biological replicates) and control RAW264.7 cells (shNT RAW264.7 cells, n = 3 biological replicates) were obtained for RNA-seq analysis; f Volcano plot showing results from differential expression analysis. Genes with P-adjusted value < 0.05 are highlighted in red or blue; g Bar plot showing the GSEA results in sh Dpep2 vs shNT RAW264.7 cells. h – k Levels of interleukin (IL)-1β, IL-6 and tumor necrosis factor-α (TNF) in sh Dpep2 vs shNT BMDMs and Dpep2 knockout ( Dpep2 KO) vs wild type (WT) mice derived BMDMs were analyzed ( n = 3 biological replicates). l, m IL-1β, IL-6 and TNF secretion of sh Dpep2 vs shNT RAW264.7 cells and Dpep2 KO vs WT mice derived BMDMs were analyzed at 24 h after LPS stimulation ( n = 3 biological replicates). n - o RAW264.7 cells and BMDMs overexpressing Dpep2 (DPEP2) and relatively control vector (Vector) cells were constructed. Levels of IL-1β, IL-6, and TNF secreted by DPEP2 cells vs Vector cells were analyzed at 24 h after LPS stimulation ( n = 3 biological replicates). Data represent the mean ± standard deviation. ns, not significant. One-way ANOVA followed by the Bonferroni multiple comparisons was used in ( a – c, e ), two-way repeated measures ANOVA with Tukey’s multiple comparisons test was used in ( d ), two-sided Wilcoxon rank-sum test was used in ( f ) and two-sided unpaired Student’s t test was used in ( h–o ). NES, n o rmalized enrichment score.

Article Snippet: RAW264.7 cells were treated with TLR1/2 ligands (1 μg/mL Pam3Csk4; HY-P1180A, MedChemExpress, Monmouth Junction, NJ, USA), TLR7/8 ligands (1 μg/mL R848; HY-13740, MedChemExpress) and TLR3 ligands (1 μg/mL poly(I:C); HY-107202, MedChemExpress) for 12 h. RAW264.7 cells, human monocytes, and BMDMs were stimulated with LPS (L4391, Sigma) to establish an in vitro inflammatory model. RAW264.7 cells were treated with LTD4 (1 μM; 20310, Cayman, Ann Arbor, MI, USA), LTE4 (1 μM; 20410, Cayman) or PGE2 (1 μM; HY-101952, MedChemExpress) in vitro.

Techniques: Derivative Assay, Control, RNA Sequencing, Quantitative Proteomics, Knock-Out, Plasmid Preparation, Construct, Standard Deviation

Journal: Journal of Human Immunity

Article Title: Novel TLR7 gain-of-function variant and review of the associated disease spectrum

doi: 10.70962/jhi.20250199

Figure Lengend Snippet: Genetic analysis of the proband. (A) De novo TLR7 mutation identified by trio-based genome sequencing. (B) Conservation of the affected proline residue across species. (C and D) Location of P435S within the extracellular domain, relative to previously reported pathogenic variants (F507S/L, P267L, Y264H). (E) NF-κB reporter assay in HEK293T cells following R848 stimulation. (F) Sustained type I interferon signaling in the TLR7-GOF patient compared to patients with monogenic type I interferonopathies. HC, healthy controls; SAVI, STING-associated vasculopathy with onset in infancy; TIR, Toll/interleukin-1 receptor/resistance protein; TM, transmembrane; ****P < 0.0001.

Article Snippet: 24 h after transfection, cells were detached, dispensed in a 96-well plate (50,000 cells/well), and left to adhere for 6 h. Transfected cells were then stimulated or not with the TLR7/8 ligand R848 (InvivoGen) at 100 ng/ml for 24 h. Luciferase activity was then measured using the Dual-Glo assay (Promega), with firefly luciferase signals normalized to Renilla luciferase activity.

Techniques: Mutagenesis, Sequencing, Residue, Reporter Assay

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tlr7 8 ligand r848 (InvivoGen)

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