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InvivoGen tlr8 agonist

(A-C) Trophoblast cells were transfected with a scramble control (control), a Let-7b-5p mimic or a Let-7b-5p inhibitor. (A) After 24 hrs and 72 hrs, Let-7b-5p expression was measured by RT-qPCR and expressed as fold change (FC) relative to the control (n=6-9; * p <0.05). (C) After 48 hrs trophoblast cell viability was measured (n=4). (C) After 48 hrs trophoblast cell migration was measured (n=6-8; * p <0.05). (D-E) Trophoblast cells were treated: (D) for 24 hrs with no treatment (NT), the TLR7 inhibitor, IRS661, or the <t>TLR8</t> inhibitor, CUCPT9a (n=9; * p <0.05), or (E) for 48hrs with NT, the TLR7 agonist, R837, or the TLR8 agonist TL8-506 (n=14; * p <0.05), after which cell migration was measured. (F) Trophoblast cells were transfected with a scramble control or a Let-7b-5p mimic and then treated with either media, IRS661 or CUCPT9a. After 24 hrs, cell migration was measured and data are shown as the fold change (FC) of trophoblast migration under Let-7b-5p mimic conditions relative to the scramble control (n=6; * p <0.05). (G) Trophoblast cells were treated with NT, IRS661 or CUCPT9a and after 24 hrs, cell viability was measured (n=3).

Tlr8 Agonist, supplied by InvivoGen, used in various techniques. Bioz Stars score: 96/100, based on 73 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/tlr8+agonist/TL8-506/bio_rxiv__64898__2026__08__03__742516-41-34-39
Average 96 stars, based on 73 article reviews

tlr8 agonist - by Bioz Stars, 2026-10

96/100 stars

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1) Product Images from "Let-7b-5p differentially regulates human first trimester trophoblast migration and sFlt-1 through TLR7 and TLR8"

Article Title: Let-7b-5p differentially regulates human first trimester trophoblast migration and sFlt-1 through TLR7 and TLR8

Journal: bioRxiv

doi: 10.64898/2026.08.03.742516

Figure Legend Snippet: (A-C) Trophoblast cells were transfected with a scramble control (control), a Let-7b-5p mimic or a Let-7b-5p inhibitor. (A) After 24 hrs and 72 hrs, Let-7b-5p expression was measured by RT-qPCR and expressed as fold change (FC) relative to the control (n=6-9; * p <0.05). (C) After 48 hrs trophoblast cell viability was measured (n=4). (C) After 48 hrs trophoblast cell migration was measured (n=6-8; * p <0.05). (D-E) Trophoblast cells were treated: (D) for 24 hrs with no treatment (NT), the TLR7 inhibitor, IRS661, or the TLR8 inhibitor, CUCPT9a (n=9; * p <0.05), or (E) for 48hrs with NT, the TLR7 agonist, R837, or the TLR8 agonist TL8-506 (n=14; * p <0.05), after which cell migration was measured. (F) Trophoblast cells were transfected with a scramble control or a Let-7b-5p mimic and then treated with either media, IRS661 or CUCPT9a. After 24 hrs, cell migration was measured and data are shown as the fold change (FC) of trophoblast migration under Let-7b-5p mimic conditions relative to the scramble control (n=6; * p <0.05). (G) Trophoblast cells were treated with NT, IRS661 or CUCPT9a and after 24 hrs, cell viability was measured (n=3).

Techniques Used: Transfection, Control, Expressing, Quantitative RT-PCR, Migration

Knock-Out:

Article Title: A TLR8 Variant Identified From Whole Exome Sequencing as a Sepsis‐Prone Mutation
Article Snippet: .. TLR8 knockout cells were generated using CRISPR‐Cas9 targeting the sg_1 guide RNA (Figure ), followed by bulk RNA sequencing after ssRNA stimulation with ssRNA40/LyoVec, a known TLR8 agonist [ ], that has been shown to be a weak TLR7 and strong TLR8 agonist when tested using cell lines expressing either human or mouse TLR7 or TLR8 ( https://www.invivogen.com/ssrna40‐lv ). ..

Generated:

CRISPR:

RNA Sequencing:

Expressing:

Incubation:

Article Title: Prostate cancer cells modulate the differentiation of THP-1 cells in response to etoposide and TLR agonists treatments.
Article Snippet: The aim of this study was to determine the polarization of macrophages in the tumor microenvironment, as well as the effect of soluble factors secreted from these polarized macrophages on etoposide-induced cancer cell apoptosis.. We investigated the effect of soluble factors secreted from the supernatant of PC3 cells treated with TLR4 and TLR8 agonists, and etoposide on macrophage polarization at protein level through flow cytometry and ELISA.. We further explored the cell cycle distribution and phagocytic activity of THP-1 cells by flow cytometry.

Article Title: Helminth products modulate innate immune recognition of nucleic acids in systemic lupus erythematosus.
Article Snippet: Aim: Current treatment of Systemic Lupus Erythematosus (SLE) is suboptimal and causes broad immunosuppression.. Therapeutic use of helminths or helminth products has been suggested for autoimmune diseases such as SLE.. In the present study, we evaluated possible immunomodulating effects of adult body fluid (ABF) from Ascaris suum on peripheral blood mononuclear cells (PBMCs) from SLE patients in an ex vivo setup.

Transfection:

Article Title: Let-7b-5p differentially regulates human first trimester trophoblast migration and sFlt-1 through TLR7 and TLR8
Article Snippet: For some experiments, 1 hr post-transfection, cells were treated with or without the TLR7 inhibitor, IRS661 (5μM; made endotoxin-free by the Keck Core, Yale University) [ , ], the TLR8 inhibitor, CUCPT9a (2.5μM) (Invivogen; San Diego, CA), or the NFκB inhibitor, BAY117085 (1μM) (Millipore-Sigma, Burlington, MA). .. In other experiments, trophoblast cells, in the absence of any transfection, were treated with either no treatment (NT), IRS661 at 5μM, CUCPT9a at 2.5 μM, the TLR7 agonist, R837 at 5μg/ml (Invivogen), or the TLR8 agonist, TL8-506 at 5μg/ml (Invivogen). .. All transfections and treatments were performed in serum-free OptiMEM (Life Technologies).

other:

Article Title: Stimulus-response signaling dynamics characterize macrophage polarization states.
Article Snippet: Trajectory data generated from microscopy experiments have been deposited at Mendeley Data: https://doi.org/10.17632/gkxzb5hcmk.1 and are publicly available as of the date of publication.

Image Search Results

Journal: bioRxiv

Article Title: Let-7b-5p differentially regulates human first trimester trophoblast migration and sFlt-1 through TLR7 and TLR8

doi: 10.64898/2026.08.03.742516

Figure Lengend Snippet: (A-C) Trophoblast cells were transfected with a scramble control (control), a Let-7b-5p mimic or a Let-7b-5p inhibitor. (A) After 24 hrs and 72 hrs, Let-7b-5p expression was measured by RT-qPCR and expressed as fold change (FC) relative to the control (n=6-9; * p <0.05). (C) After 48 hrs trophoblast cell viability was measured (n=4). (C) After 48 hrs trophoblast cell migration was measured (n=6-8; * p <0.05). (D-E) Trophoblast cells were treated: (D) for 24 hrs with no treatment (NT), the TLR7 inhibitor, IRS661, or the TLR8 inhibitor, CUCPT9a (n=9; * p <0.05), or (E) for 48hrs with NT, the TLR7 agonist, R837, or the TLR8 agonist TL8-506 (n=14; * p <0.05), after which cell migration was measured. (F) Trophoblast cells were transfected with a scramble control or a Let-7b-5p mimic and then treated with either media, IRS661 or CUCPT9a. After 24 hrs, cell migration was measured and data are shown as the fold change (FC) of trophoblast migration under Let-7b-5p mimic conditions relative to the scramble control (n=6; * p <0.05). (G) Trophoblast cells were treated with NT, IRS661 or CUCPT9a and after 24 hrs, cell viability was measured (n=3).

Article Snippet: In other experiments, trophoblast cells, in the absence of any transfection, were treated with either no treatment (NT), IRS661 at 5μM, CUCPT9a at 2.5 μM, the TLR7 agonist, R837 at 5μg/ml (Invivogen), or the TLR8 agonist, TL8-506 at 5μg/ml (Invivogen).

Techniques: Transfection, Control, Expressing, Quantitative RT-PCR, Migration

( A ) The family tree depicts individuals with the TLR8 variant. Solid black boxes represent males P1 and P2 with the germline variant, while half-black circles indicate heterozygous female carriers. ND, not determined. ( B ) Sanger sequencing of the family members’ DNA confirms the presence of the TLR8 variant. ( C ) Leucine-rich repeat (LRR) TLR8 with the Z-loop (PDB ID: 3W3G). The A518 variant in LRR 16 is highlighted in purple. Previously reported variants from Aluri et al. , Fejtkova et al. , and Liang et al. are denoted in cyan.

Journal: JCI Insight

Article Title: Structural modeling and functional characterization of a novel gain-of-function TLR8 variant causing severe inflammatory syndrome

doi: 10.1172/jci.insight.187422

Figure Lengend Snippet: ( A ) The family tree depicts individuals with the TLR8 variant. Solid black boxes represent males P1 and P2 with the germline variant, while half-black circles indicate heterozygous female carriers. ND, not determined. ( B ) Sanger sequencing of the family members’ DNA confirms the presence of the TLR8 variant. ( C ) Leucine-rich repeat (LRR) TLR8 with the Z-loop (PDB ID: 3W3G). The A518 variant in LRR 16 is highlighted in purple. Previously reported variants from Aluri et al. , Fejtkova et al. , and Liang et al. are denoted in cyan.

Article Snippet: Cells were then stimulated with either TLR8 agonists — 50 ng/mL, 100 ng/mL, or 1 μg/mL TL8-506 (tlrl-tl8506, InvivoGen) and 1 μg/mL ORN 06 (tlrl-orn6, InvivoGen) — or 1 μg/mL CL097 TLR7 agonist.

Techniques: Variant Assay, Sequencing

( A ) Ribbon diagram of the side view of TLR8 receptor homodimer (PDB ID: 4R08) with the 2 chains colored gray and pink, and residue 518 indicated in a purple halo, positioned at the interface of the homodimer and the uridine residue in ball-and-stick representation in orange with an orange halo. ( B ) Comparison of hydrogen bonds in the WT protein (left) and A518T variant (right). The hydrogen bonds that are conserved in both proteins are shown as red dashed lines, and the additional hydrogen bonds formed by the A518T variant are shown as black dashed lines and a blue halo. A gray rectangle highlights the differences in hydrogen bonding patterns in the WT and A518T variant proteins. The uridine residue (URI) is represented with ball and stick in orange with an orange halo around it, and the atoms are colored according to the elements with red and blue spheres representing oxygen and nitrogen, respectively. The hydrogen-bonded residues are numbered and shown with ball-and-stick representation with their respective 3-letter codes. ( C ) Comparison of the Δ vibrational entropy energy of A518T variant with respect to the WT protein in the ligand-bound activated state (green) and the unbound inactivated state (blue) with the residue numbers on the x axis, calculated by DynaMut. ( D ) Comparison of water-mediated interchain hydrogen bonds in the WT protein in the activated state (dark gray), WT protein in the inactivated state (light gray), A518T variant in the activated state (blue), and A518T variant in the inactivated state (green), based on molecular dynamics simulations with OpenMM.

Journal: JCI Insight

Article Title: Structural modeling and functional characterization of a novel gain-of-function TLR8 variant causing severe inflammatory syndrome

doi: 10.1172/jci.insight.187422

Figure Lengend Snippet: ( A ) Ribbon diagram of the side view of TLR8 receptor homodimer (PDB ID: 4R08) with the 2 chains colored gray and pink, and residue 518 indicated in a purple halo, positioned at the interface of the homodimer and the uridine residue in ball-and-stick representation in orange with an orange halo. ( B ) Comparison of hydrogen bonds in the WT protein (left) and A518T variant (right). The hydrogen bonds that are conserved in both proteins are shown as red dashed lines, and the additional hydrogen bonds formed by the A518T variant are shown as black dashed lines and a blue halo. A gray rectangle highlights the differences in hydrogen bonding patterns in the WT and A518T variant proteins. The uridine residue (URI) is represented with ball and stick in orange with an orange halo around it, and the atoms are colored according to the elements with red and blue spheres representing oxygen and nitrogen, respectively. The hydrogen-bonded residues are numbered and shown with ball-and-stick representation with their respective 3-letter codes. ( C ) Comparison of the Δ vibrational entropy energy of A518T variant with respect to the WT protein in the ligand-bound activated state (green) and the unbound inactivated state (blue) with the residue numbers on the x axis, calculated by DynaMut. ( D ) Comparison of water-mediated interchain hydrogen bonds in the WT protein in the activated state (dark gray), WT protein in the inactivated state (light gray), A518T variant in the activated state (blue), and A518T variant in the inactivated state (green), based on molecular dynamics simulations with OpenMM.

Techniques: Residue, Comparison, Variant Assay

( A ) Histogram plots of p–NF-κB of CD45 + CD14 + monocytes from freshly isolated PBMCs in family members relative to healthy males (CTRm; n = 3) (left) with the corresponding MFI (right). Data represent mean ± SEM for healthy male controls. ( B ) Histogram plots of TLR8 of CD45 + CD14 + monocytes from freshly isolated PBMCs in family members relative to healthy males (CTRm; n = 3) (left) and the ratio of ∆ p–NF-κB + to TLR8 + of CD45 + CD14 + monocytes (right). Data represent mean ± SEM for healthy male controls. ( C ) Volcano plot illustrating differentially expressed genes in unstimulated CD14 + CD16 – monocytes isolated from healthy male controls ( n = 4) compared with family members (P1 and P2). Genes with significant upregulation and downregulation are highlighted based on adjusted P values and fold change thresholds. ( D ) Bubble plot representing the top enriched pathways identified from the differentially expressed genes. Bubble size corresponds to the percentage of genes involved, and color intensity reflects the significance of pathway enrichment.

Journal: JCI Insight

Article Title: Structural modeling and functional characterization of a novel gain-of-function TLR8 variant causing severe inflammatory syndrome

doi: 10.1172/jci.insight.187422

Figure Lengend Snippet: ( A ) Histogram plots of p–NF-κB of CD45 + CD14 + monocytes from freshly isolated PBMCs in family members relative to healthy males (CTRm; n = 3) (left) with the corresponding MFI (right). Data represent mean ± SEM for healthy male controls. ( B ) Histogram plots of TLR8 of CD45 + CD14 + monocytes from freshly isolated PBMCs in family members relative to healthy males (CTRm; n = 3) (left) and the ratio of ∆ p–NF-κB + to TLR8 + of CD45 + CD14 + monocytes (right). Data represent mean ± SEM for healthy male controls. ( C ) Volcano plot illustrating differentially expressed genes in unstimulated CD14 + CD16 – monocytes isolated from healthy male controls ( n = 4) compared with family members (P1 and P2). Genes with significant upregulation and downregulation are highlighted based on adjusted P values and fold change thresholds. ( D ) Bubble plot representing the top enriched pathways identified from the differentially expressed genes. Bubble size corresponds to the percentage of genes involved, and color intensity reflects the significance of pathway enrichment.

Techniques: Isolation

( A ) Western blot against TLR8, p–NF-κB, total NF-κB, and γ-tubulin (γ-TUB) in BlaER1 TLR8 –/– cells with the insertion of the TLR8 WT protein or the p.A518T and the previously published p.D543A (loss-of-function) TLR8 variants. Cells were stimulated with 100 ng/mL TL8-506 agonist for 15 minutes (left), and the ratio of p–NF-κB to total NF-κB to TLR8 levels, normalized to TLR8 levels, is shown (right). Statistical significance between groups was assessed using a 2-way ANOVA multiple-comparison test. Data represent mean ± SEM of n = 4 experiments. RQ, relative quantification. ( B ) IL-6 quantification of BlaER1 TLR8 –/– cells with the insertion of the TLR8 WT protein or the p.A518T and p.D543A (loss-of-function) variants. Cells were stimulated with 1 μg/mL TL8-506 and 1 μg/mL ORN 06 agonists. Data are presented after the subtraction of the unstimulated measurements. Statistical significance between groups was assessed using a 2-way ANOVA multiple-comparison test. Data represent mean ± SEM of n = 3–4 experiments. Differences between groups were considered significant at P values less than 0.05.

Journal: JCI Insight

Article Title: Structural modeling and functional characterization of a novel gain-of-function TLR8 variant causing severe inflammatory syndrome

doi: 10.1172/jci.insight.187422

Figure Lengend Snippet: ( A ) Western blot against TLR8, p–NF-κB, total NF-κB, and γ-tubulin (γ-TUB) in BlaER1 TLR8 –/– cells with the insertion of the TLR8 WT protein or the p.A518T and the previously published p.D543A (loss-of-function) TLR8 variants. Cells were stimulated with 100 ng/mL TL8-506 agonist for 15 minutes (left), and the ratio of p–NF-κB to total NF-κB to TLR8 levels, normalized to TLR8 levels, is shown (right). Statistical significance between groups was assessed using a 2-way ANOVA multiple-comparison test. Data represent mean ± SEM of n = 4 experiments. RQ, relative quantification. ( B ) IL-6 quantification of BlaER1 TLR8 –/– cells with the insertion of the TLR8 WT protein or the p.A518T and p.D543A (loss-of-function) variants. Cells were stimulated with 1 μg/mL TL8-506 and 1 μg/mL ORN 06 agonists. Data are presented after the subtraction of the unstimulated measurements. Statistical significance between groups was assessed using a 2-way ANOVA multiple-comparison test. Data represent mean ± SEM of n = 3–4 experiments. Differences between groups were considered significant at P values less than 0.05.

Techniques: Western Blot, Comparison, Quantitative Proteomics

( A ) Western blot against TLR8, γ-TUB, and lactate dehydrogenase A (LDHA) of cycloheximide-incubated (CHX-incubated) HEK BN1 cells expressing TLR8 WT or the p.A518T and the previously published p.G572V (gain-of-function) variants (left), and Western blot quantification (right). Statistical significance between groups was assessed using a 2-way ANOVA multiple-comparison test. Data represent mean ± SEM of n = 4 experiments. ( B ) Western blot analysis of HA-tagged immunoprecipitated proteins from HEK293T cell extracts treated with (+) or without (–) the proteasome inhibitor MG132 and CHX. Cells were transfected with HA-tagged constructs and subjected to immunoprecipitation using anti-HA antibody. Left: Blots were probed with antibodies against ubiquitin, TLR8, and the HA tag to assess protein ubiquitination, TLR8 levels, and expression of the HA-tagged construct. Right: Quantification of ubiquitin signal normalized to TLR8 (top) and to HA (bottom) signals, showing the relative levels of TLR8 ubiquitination and overall ubiquitination of HA-tagged proteins. Statistical significance was assessed with a 2-way ANOVA multiple-comparison test. Data represent mean ± SEM of n = 3 experiments. Differences between groups were considered significant at P values less than 0.05.

Journal: JCI Insight

Article Title: Structural modeling and functional characterization of a novel gain-of-function TLR8 variant causing severe inflammatory syndrome

doi: 10.1172/jci.insight.187422

Figure Lengend Snippet: ( A ) Western blot against TLR8, γ-TUB, and lactate dehydrogenase A (LDHA) of cycloheximide-incubated (CHX-incubated) HEK BN1 cells expressing TLR8 WT or the p.A518T and the previously published p.G572V (gain-of-function) variants (left), and Western blot quantification (right). Statistical significance between groups was assessed using a 2-way ANOVA multiple-comparison test. Data represent mean ± SEM of n = 4 experiments. ( B ) Western blot analysis of HA-tagged immunoprecipitated proteins from HEK293T cell extracts treated with (+) or without (–) the proteasome inhibitor MG132 and CHX. Cells were transfected with HA-tagged constructs and subjected to immunoprecipitation using anti-HA antibody. Left: Blots were probed with antibodies against ubiquitin, TLR8, and the HA tag to assess protein ubiquitination, TLR8 levels, and expression of the HA-tagged construct. Right: Quantification of ubiquitin signal normalized to TLR8 (top) and to HA (bottom) signals, showing the relative levels of TLR8 ubiquitination and overall ubiquitination of HA-tagged proteins. Statistical significance was assessed with a 2-way ANOVA multiple-comparison test. Data represent mean ± SEM of n = 3 experiments. Differences between groups were considered significant at P values less than 0.05.

Techniques: Western Blot, Incubation, Expressing, Comparison, Immunoprecipitation, Transfection, Construct, Ubiquitin Proteomics

Dynamics of immune cell subsets in response to agonist stimulation. A Schematic of the experimental workflow. Immune profiling by flow cytometry was performed 48 h after a single intratumoral injection of PRR agonists. B Percentage of CD45 + leukocytes among live cells following intratumoral administration of different agonists: TLR3 agonist poly IC (25 µg/tumor), TLR7 agonist imiquimod hydrochloride (25 µg/tumor), TLR8 agonist TL8-506 (10 µg/tumor), TLR9 agonist CpG ODN 2395 (50 µg/tumor), STING agonist ADU-S100 ammonium salt (25 µg/tumor), NOD1 agonist Tri-DAP (10 µg/tumor), and NOD2 agonist murabutide (5 µg/tumor). C Proportion of cDCs within the CD45 + population. D Percentage of ZsGreen + cells among DCs. E Proportion of macrophages within the CD45 + population. F Percentage of ZsGreen + cells among macrophages. G Proportion of CD8 + T cells within the CD45 + compartment. H Proportion of cCD4 + T cells within the CD45 + compartment. I Proportion of Tregs within the CD45 + compartment, pooled from two independent experiments. J Ratio of cCD4 + T cells to Tregs. (K) Ratio of CD8 + T cells to Tregs. Data represent the mean ± SEM ( n = 8 mice per group). Statistical comparisons were performed using one-way ANOVA. * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001

Journal: Cancer Immunology, Immunotherapy : CII

Article Title: TLR8 agonists remodel the tumor immune microenvironment through PF4-dependent T cell recruitment and ancillary mechanisms

doi: 10.1007/s00262-026-04329-8

Figure Lengend Snippet: Dynamics of immune cell subsets in response to agonist stimulation. A Schematic of the experimental workflow. Immune profiling by flow cytometry was performed 48 h after a single intratumoral injection of PRR agonists. B Percentage of CD45 + leukocytes among live cells following intratumoral administration of different agonists: TLR3 agonist poly IC (25 µg/tumor), TLR7 agonist imiquimod hydrochloride (25 µg/tumor), TLR8 agonist TL8-506 (10 µg/tumor), TLR9 agonist CpG ODN 2395 (50 µg/tumor), STING agonist ADU-S100 ammonium salt (25 µg/tumor), NOD1 agonist Tri-DAP (10 µg/tumor), and NOD2 agonist murabutide (5 µg/tumor). C Proportion of cDCs within the CD45 + population. D Percentage of ZsGreen + cells among DCs. E Proportion of macrophages within the CD45 + population. F Percentage of ZsGreen + cells among macrophages. G Proportion of CD8 + T cells within the CD45 + compartment. H Proportion of cCD4 + T cells within the CD45 + compartment. I Proportion of Tregs within the CD45 + compartment, pooled from two independent experiments. J Ratio of cCD4 + T cells to Tregs. (K) Ratio of CD8 + T cells to Tregs. Data represent the mean ± SEM ( n = 8 mice per group). Statistical comparisons were performed using one-way ANOVA. * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001

Article Snippet: When tumors reached approximately 200 mm 3 , PRR agonists were administered via intratumoral injection at the following doses: TLR3 agonist poly(I:C) (Sigma-Aldrich, #42,424–50-0; 25 μg/tumor); TLR7 agonist imiquimod hydrochloride (MedChemExpress, #HY-B0180A; 25 μg/tumor); TLR8 agonist TL8-506 (InvivoGen, #tlrl-tl8506; 10 μg/tumor); TLR8 agonist motolimod (MedChemExpress, #HY-13773; 50 μg/tumor); TLR9 agonist CpG ODN 2395 (Class C) (InvivoGen, #tlrl-2395–1; 50 μg/tumor); STING agonist ADU-S100 ammonium salt (MedChemExpress, #HY-12885B; 25 μg/tumor); NOD1 agonist Tri-DAP (InvivoGen, #tlrl-tdap; 10 μg/tumor); and NOD2 agonist murabutide (InvivoGen, #tlrl-mbt; 5 μg/tumor).

Techniques: Flow Cytometry, Injection

Immune modulation and antitumor effects of TLR8 agonists. A Flow cytometric analysis of CD45 + leukocytes was performed 48 h after three intratumoral injections of TL8-506 (10 µg/tumor) or motolimod (50 µg/tumor) ( n = 6). B Percentage of cDCs within the CD45 + population and proportion of ZsGreen + cells among cDCs ( n = 6). C Percentage of macrophages within the CD45 + population and proportion of ZsGreen + cells among macrophages ( n = 6). D Frequency of cCD4 + T cells, CD8 + T cells, and Tregs within the CD45 + compartment ( n = 6). E Ratios of cCD4 + T cells to Tregs and CD8 T cells to Tregs ( n = 6). F , G Tumor growth curves and terminal tumor weights of AKR and MC38 tumors in C57BL/6 mice administered TL8-506 or motolimod every 3 days ( n = 5). H , I Tumor growth curves and terminal tumor weights of AKR and MC38 tumors in nude mice administered motolimod every three days ( n = 5). J , K Macrophage phagocytosis of CFSE-labeled tumor cells following motolimod stimulation ( n = 5). Data represent the mean ± SEM. Data in panels A–G were analyzed using one-way ANOVA, and data in panels H–K were analyzed using Student’s t-tests. * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001

Journal: Cancer Immunology, Immunotherapy : CII

Article Title: TLR8 agonists remodel the tumor immune microenvironment through PF4-dependent T cell recruitment and ancillary mechanisms

doi: 10.1007/s00262-026-04329-8

Figure Lengend Snippet: Immune modulation and antitumor effects of TLR8 agonists. A Flow cytometric analysis of CD45 + leukocytes was performed 48 h after three intratumoral injections of TL8-506 (10 µg/tumor) or motolimod (50 µg/tumor) ( n = 6). B Percentage of cDCs within the CD45 + population and proportion of ZsGreen + cells among cDCs ( n = 6). C Percentage of macrophages within the CD45 + population and proportion of ZsGreen + cells among macrophages ( n = 6). D Frequency of cCD4 + T cells, CD8 + T cells, and Tregs within the CD45 + compartment ( n = 6). E Ratios of cCD4 + T cells to Tregs and CD8 T cells to Tregs ( n = 6). F , G Tumor growth curves and terminal tumor weights of AKR and MC38 tumors in C57BL/6 mice administered TL8-506 or motolimod every 3 days ( n = 5). H , I Tumor growth curves and terminal tumor weights of AKR and MC38 tumors in nude mice administered motolimod every three days ( n = 5). J , K Macrophage phagocytosis of CFSE-labeled tumor cells following motolimod stimulation ( n = 5). Data represent the mean ± SEM. Data in panels A–G were analyzed using one-way ANOVA, and data in panels H–K were analyzed using Student’s t-tests. * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001

Techniques: Labeling

TLR8 agonist activates PF4-CXCR3 pathway to shape the TIME. A t-SNE plot showing the distribution of all cells from the control and agonist-treated groups combined ( n = 15,745 cells). B t-SNE plot depicting the distribution of distinct immune cell types. C Dot plot displaying the marker genes used to define each immune cell population. D Density plot showing the distribution of Tlr8-expressing cells across the t-SNE map. E Violin plot illustrating Tlr8 expression levels across different immune cell types. F Circle plot depicting the strength of Pf4–Cxcr3 receptor–ligand interactions between distinct cell types in the control and motolimod-treated groups. G Differential gene expression profiles of neutrophils, macrophages, cDC2, and CD8 + T cells. H Bubble plot comparing changes in specific receptor–ligand interactions between the control and motolimod-treated groups, focusing on macrophage-to-cCD4 + T signaling, cDC2-to-cCD4 + T signaling, and CD8 + T-to-cCD4 + T signaling. I Violin plot showing differential expression of Cxcr3 in cCD4 + T and Tregs, analyzed using the Wilcoxon rank-sum test. ns, not significant; ** P < 0.01

Journal: Cancer Immunology, Immunotherapy : CII

Article Title: TLR8 agonists remodel the tumor immune microenvironment through PF4-dependent T cell recruitment and ancillary mechanisms

doi: 10.1007/s00262-026-04329-8

Figure Lengend Snippet: TLR8 agonist activates PF4-CXCR3 pathway to shape the TIME. A t-SNE plot showing the distribution of all cells from the control and agonist-treated groups combined ( n = 15,745 cells). B t-SNE plot depicting the distribution of distinct immune cell types. C Dot plot displaying the marker genes used to define each immune cell population. D Density plot showing the distribution of Tlr8-expressing cells across the t-SNE map. E Violin plot illustrating Tlr8 expression levels across different immune cell types. F Circle plot depicting the strength of Pf4–Cxcr3 receptor–ligand interactions between distinct cell types in the control and motolimod-treated groups. G Differential gene expression profiles of neutrophils, macrophages, cDC2, and CD8 + T cells. H Bubble plot comparing changes in specific receptor–ligand interactions between the control and motolimod-treated groups, focusing on macrophage-to-cCD4 + T signaling, cDC2-to-cCD4 + T signaling, and CD8 + T-to-cCD4 + T signaling. I Violin plot showing differential expression of Cxcr3 in cCD4 + T and Tregs, analyzed using the Wilcoxon rank-sum test. ns, not significant; ** P < 0.01

Techniques: Control, Marker, Expressing, Gene Expression, Quantitative Proteomics

TLR8 agonist induces PF4 expression through NF-κB signaling pathway. A , B qRT-PCR analysis of Pf4 expression in mouse and human macrophages in the motolimod-treated and control groups ( n = 3). C , D Luminescence assay showing NF-κB pathway activation in mouse and human macrophages following motolimod stimulation ( n = 3). E , F qRT-PCR analysis of Rela expression in Rela -knockdown and control mouse and human macrophages with or without motolimod treatment ( n = 3). G , H Western blotting showing p65 protein levels in RELA -knockdown and control mouse and human macrophages with or without motolimod treatment. I , J qRT-PCR analysis of Pf4 / PF4 expression in Rela / RELA -knockdown and control mouse and human macrophages with or without motolimod treatment ( n = 3). K ELISA quantification of Pf4 levels in the culture supernatant from Rela -knockdown and control mouse macrophages with or without motolimod treatment ( n = 3). Data represent the mean ± SEM. Statistical comparisons were performed using Student’s t-tests. * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001

Journal: Cancer Immunology, Immunotherapy : CII

Article Title: TLR8 agonists remodel the tumor immune microenvironment through PF4-dependent T cell recruitment and ancillary mechanisms

doi: 10.1007/s00262-026-04329-8

Figure Lengend Snippet: TLR8 agonist induces PF4 expression through NF-κB signaling pathway. A , B qRT-PCR analysis of Pf4 expression in mouse and human macrophages in the motolimod-treated and control groups ( n = 3). C , D Luminescence assay showing NF-κB pathway activation in mouse and human macrophages following motolimod stimulation ( n = 3). E , F qRT-PCR analysis of Rela expression in Rela -knockdown and control mouse and human macrophages with or without motolimod treatment ( n = 3). G , H Western blotting showing p65 protein levels in RELA -knockdown and control mouse and human macrophages with or without motolimod treatment. I , J qRT-PCR analysis of Pf4 / PF4 expression in Rela / RELA -knockdown and control mouse and human macrophages with or without motolimod treatment ( n = 3). K ELISA quantification of Pf4 levels in the culture supernatant from Rela -knockdown and control mouse macrophages with or without motolimod treatment ( n = 3). Data represent the mean ± SEM. Statistical comparisons were performed using Student’s t-tests. * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001

Techniques: Expressing, Quantitative RT-PCR, Control, Luminescence Assay, Activation Assay, Knockdown, Western Blot, Enzyme-linked Immunosorbent Assay

TLR8 agonist enhances the efficacy of anti-PD-1 therapy. A Experimental workflow showing treatment schedule for AKR tumor-bearing C57BL/6 mice receiving intratumoral motolimod and intraperitoneal anti-PD-1 (αPD-1) antibody, alone or in combination. B , C Tumor growth curves and survival analysis of AKR tumor-bearing mice treated with the indicated regimens ( n = 7 mice per group). D Experimental workflow showing treatment schedule and details for MC38 tumors in C57BL/6 mice receiving intratumoral motolimod and intraperitoneal αPD-1 antibody, alone or in combination. E , F Tumor growth curves and survival analysis of MC38 tumor-bearing mice treated with the indicated regimens ( n = 7 mice per group). Data represent the mean ± SEM. Tumor growth curves were analyzed using one-way ANOVA, and survival curves were analyzed using log-rank testing. * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001

Journal: Cancer Immunology, Immunotherapy : CII

Article Title: TLR8 agonists remodel the tumor immune microenvironment through PF4-dependent T cell recruitment and ancillary mechanisms

doi: 10.1007/s00262-026-04329-8

Figure Lengend Snippet: TLR8 agonist enhances the efficacy of anti-PD-1 therapy. A Experimental workflow showing treatment schedule for AKR tumor-bearing C57BL/6 mice receiving intratumoral motolimod and intraperitoneal anti-PD-1 (αPD-1) antibody, alone or in combination. B , C Tumor growth curves and survival analysis of AKR tumor-bearing mice treated with the indicated regimens ( n = 7 mice per group). D Experimental workflow showing treatment schedule and details for MC38 tumors in C57BL/6 mice receiving intratumoral motolimod and intraperitoneal αPD-1 antibody, alone or in combination. E , F Tumor growth curves and survival analysis of MC38 tumor-bearing mice treated with the indicated regimens ( n = 7 mice per group). Data represent the mean ± SEM. Tumor growth curves were analyzed using one-way ANOVA, and survival curves were analyzed using log-rank testing. * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001

Techniques:

HuTLR8 induces fetal resorption and spontaneous pregnancy loss in Sle1 mice. A) C57Bl/6.huTLR8tg mice were crossed with Yaa males and then with Sle1 females . Sle1.huTLR8tg female mice express one (Sle1.huTLR8 +/- ) or two (Sle1.huTLR8 +/+ ) copies of the single human TLR8 (huTLR8) transgenic locus. B. Outcomes of observed pregnancies. Adverse outcome was defined as maternal distress or death at delivery with evidence of an impacted pup or birth of dead or runted pups. p values calculated using Chi square analysis. C. I. An impacted pup in a Sle1.huTLR8 +/+ female II. An impacted pup together with an unaffected littermate; III. Representative uteri from Sle1 (top) and Sle1.huTLR8 +/+ (bottom) mice; IV. Growth retarded pup with an associated small placenta (*); V. A normal sized fetus and a resorbed fetus from the same pregnancy. D. Fetal weights (in gram) are depicted for full term Sle1 (n=5) and C57BL/6.huTLR8tg control live pregnancies and Sle1.huTLR8 +/- (n=16) and Sle1.huTLR8 +/+ (n=18) pregnancies with dystocia. Impacted/resorbed/dead fetuses are depicted in red. Maternal genotype and number of pregnancies are shown below the x axis. E, F. Total number of pups (E) and number of male (blue bars) and female (pink bars) pups (F) per live litter. Maternal genotype and number of pregnancies are shown below the x axis. Each symbol represents an individual pregnancy; bars represent the mean + SD. D-F: p values calculated using Kruskal Wallis ANOVA with Dunn’s correction for multiple analyses. *p<0.05; **p<0.01; ***p<0.001; ****p<0.0001.

Journal: bioRxiv

Article Title: Pregnancy loss due to early developmental defects in lupus mice expressing human TLR8

doi: 10.64898/2026.02.07.701591

Figure Lengend Snippet: HuTLR8 induces fetal resorption and spontaneous pregnancy loss in Sle1 mice. A) C57Bl/6.huTLR8tg mice were crossed with Yaa males and then with Sle1 females . Sle1.huTLR8tg female mice express one (Sle1.huTLR8 +/- ) or two (Sle1.huTLR8 +/+ ) copies of the single human TLR8 (huTLR8) transgenic locus. B. Outcomes of observed pregnancies. Adverse outcome was defined as maternal distress or death at delivery with evidence of an impacted pup or birth of dead or runted pups. p values calculated using Chi square analysis. C. I. An impacted pup in a Sle1.huTLR8 +/+ female II. An impacted pup together with an unaffected littermate; III. Representative uteri from Sle1 (top) and Sle1.huTLR8 +/+ (bottom) mice; IV. Growth retarded pup with an associated small placenta (*); V. A normal sized fetus and a resorbed fetus from the same pregnancy. D. Fetal weights (in gram) are depicted for full term Sle1 (n=5) and C57BL/6.huTLR8tg control live pregnancies and Sle1.huTLR8 +/- (n=16) and Sle1.huTLR8 +/+ (n=18) pregnancies with dystocia. Impacted/resorbed/dead fetuses are depicted in red. Maternal genotype and number of pregnancies are shown below the x axis. E, F. Total number of pups (E) and number of male (blue bars) and female (pink bars) pups (F) per live litter. Maternal genotype and number of pregnancies are shown below the x axis. Each symbol represents an individual pregnancy; bars represent the mean + SD. D-F: p values calculated using Kruskal Wallis ANOVA with Dunn’s correction for multiple analyses. *p<0.05; **p<0.01; ***p<0.001; ****p<0.0001.

Article Snippet: Bone marrow neutrophils were isolated from 3– and 6-month-old homozygous female Sle1.huTLR8tg, Sle1 and C57BL/6 controls using EasySep mouse neutrophil enrichment kit (STEMCELL) and were treated with PMA 50nM for 4 hours at 37°C with or without pre-treatment with PMA or TLR8 agonist CL075 (Invivogen) 10mg/ml for 20 minutes.

Techniques: Transgenic Assay, Control

SARS-CoV-2 Delta and Omicron BA.1 variants induce robust gene expression changes in human pDCs RNAseq analysis of pDC purified population, stimulated for 20 h by Medium, R848, Delta or Omicron BA.1 SARS-CoV-2 variants. (A) Experimental workflow (Created with BioRender.com ). (B) Stacked bar chart showing the number of differentially expressed genes (DEGs, adjusted p value <0.05) in pDCs after 20 h stimulation with Delta, Omicron BA.1, or R848 compared to unstimulated control. (C) Venn diagrams of the intersection of up and down differentially expressed genes across Delta, Omicron, and R848 treatments, revealing both common and stimulus-specific transcriptional signatures. (D) Pathway enrichment analysis of the core transcriptional signature shared by SARS-CoV-2 Delta and Omicron BA.1 variants in pDCs. (E) Expression heatmap of functionally categorized genes with robust upregulation of interferon-stimulated genes (ISGs), chemokines, and inflammatory mediators across Delta, Omicron BA.1, and R848 stimulations, highlighting the core antiviral response signature in pDCs. (F) Pathway enrichment analysis revealing virus-specific activation of multiple recognition pathways (endosomal and cytoplasmic sensors) compared to PKR and direct TLR7/8-restricted signaling by R848.

Journal: iScience

Article Title: Differential response of human plasmacytoid pre-dendritic cells to SARS-CoV-2 variants

doi: 10.1016/j.isci.2025.113394

Figure Lengend Snippet: SARS-CoV-2 Delta and Omicron BA.1 variants induce robust gene expression changes in human pDCs RNAseq analysis of pDC purified population, stimulated for 20 h by Medium, R848, Delta or Omicron BA.1 SARS-CoV-2 variants. (A) Experimental workflow (Created with BioRender.com ). (B) Stacked bar chart showing the number of differentially expressed genes (DEGs, adjusted p value <0.05) in pDCs after 20 h stimulation with Delta, Omicron BA.1, or R848 compared to unstimulated control. (C) Venn diagrams of the intersection of up and down differentially expressed genes across Delta, Omicron, and R848 treatments, revealing both common and stimulus-specific transcriptional signatures. (D) Pathway enrichment analysis of the core transcriptional signature shared by SARS-CoV-2 Delta and Omicron BA.1 variants in pDCs. (E) Expression heatmap of functionally categorized genes with robust upregulation of interferon-stimulated genes (ISGs), chemokines, and inflammatory mediators across Delta, Omicron BA.1, and R848 stimulations, highlighting the core antiviral response signature in pDCs. (F) Pathway enrichment analysis revealing virus-specific activation of multiple recognition pathways (endosomal and cytoplasmic sensors) compared to PKR and direct TLR7/8-restricted signaling by R848.

Article Snippet: TLR7/TLR8 agonist R848 (Resiquimod) , InvivoGen , Ref. tlrl-r848-1.

Techniques: Gene Expression, Purification, Control, Expressing, Virus, Activation Assay

SARS-CoV-2 variant BA.1 shifts human pDCs differentiation to P3 phenotype. pDC activation by SARS-CoV-2 variants is dose-dependent and variant-dependent (A) Human pDC diversification, (defined by PDL1 and CD80 expression) upon Medium, R848 or SARS-CoV-2 variants (MOI = 4) stimulation. Representative plots from 1 healthy donor out of 5 is shown. (B) Quantification of P1, P2, P3 sub-populations in stimulated pDC. Five healthy donors from three independent experiment are shown. (C) Superposed dot plot of Unsupervised FlowSom analysis of concatenated samples of pDC+ Delta or BA.1 (MOI = 4, n = 8). (D) Human pDC were stimulated with SARS-CoV-2 variants at different concentrations (MOI = 0.08, 0.4, 4, and 12). The % of P3 pDC was assessed by flow cytometry based on PD-L1 and CD80 expression. Five healthy donors from three independent experiment are shown. (E ) Same experiment than D except that pDC were co-cultured 20 h with Vero cells infected with SARS CoV-2 variants (3, 10, 25, and 45% of infected vero cells/pDC, P3, and P1 are presented). Four healthy donors are shown. Histograms represent means and bars SD. ∗, p < 0.05; ∗∗, p < 0.01; B— Mann-Whitney test; D, E two-way ANOVA test with Geisser-Greenhouse correction. Bars represent means ± SD.

Journal: iScience

Article Title: Differential response of human plasmacytoid pre-dendritic cells to SARS-CoV-2 variants

doi: 10.1016/j.isci.2025.113394

Figure Lengend Snippet: SARS-CoV-2 variant BA.1 shifts human pDCs differentiation to P3 phenotype. pDC activation by SARS-CoV-2 variants is dose-dependent and variant-dependent (A) Human pDC diversification, (defined by PDL1 and CD80 expression) upon Medium, R848 or SARS-CoV-2 variants (MOI = 4) stimulation. Representative plots from 1 healthy donor out of 5 is shown. (B) Quantification of P1, P2, P3 sub-populations in stimulated pDC. Five healthy donors from three independent experiment are shown. (C) Superposed dot plot of Unsupervised FlowSom analysis of concatenated samples of pDC+ Delta or BA.1 (MOI = 4, n = 8). (D) Human pDC were stimulated with SARS-CoV-2 variants at different concentrations (MOI = 0.08, 0.4, 4, and 12). The % of P3 pDC was assessed by flow cytometry based on PD-L1 and CD80 expression. Five healthy donors from three independent experiment are shown. (E ) Same experiment than D except that pDC were co-cultured 20 h with Vero cells infected with SARS CoV-2 variants (3, 10, 25, and 45% of infected vero cells/pDC, P3, and P1 are presented). Four healthy donors are shown. Histograms represent means and bars SD. ∗, p < 0.05; ∗∗, p < 0.01; B— Mann-Whitney test; D, E two-way ANOVA test with Geisser-Greenhouse correction. Bars represent means ± SD.

Article Snippet: TLR7/TLR8 agonist R848 (Resiquimod) , InvivoGen , Ref. tlrl-r848-1.

Techniques: Variant Assay, Activation Assay, Expressing, Flow Cytometry, Cell Culture, Infection, MANN-WHITNEY

СD4 + naive T cells underwent a stronger differentiation into robust effector T cells when primed with pDC stimulated with Omicron BA.1 (A) Experimental schema (Created with BioRender.com ). (B) Histogram of CFSE cell trace expression by T cells after 7 days of co-culture, as well as CD45RA expression in CFSE negative and positive population (C). Representative plots of CD3 + CD4 + CD25 + CD45RA − T cells (D). Quantification of CD3 + CD4 + CFSE − CD25 + CD45RA − T cells of allogenic co-culture (E). Geometric mean of fluorescence intensity for CD45RA, CD25, PD1 surface markers on T cells (F). IL-2, IL-13, GMCSF, IFN- γ , IL-10 and IL-5 cytokine secretion by T cells after 7 days of allogenic co-culture with pDC stimulated with Medium, R848, and Delta or BA.1 SARS-CoV-2 viral variants. n = 8 healthy donors from 5 independent experiments. ∗, p < 0.05; ∗∗, p < 0.01; Mann-Whitney test. Bars represent means ± SD.

Journal: iScience

Article Title: Differential response of human plasmacytoid pre-dendritic cells to SARS-CoV-2 variants

doi: 10.1016/j.isci.2025.113394

Figure Lengend Snippet: СD4 + naive T cells underwent a stronger differentiation into robust effector T cells when primed with pDC stimulated with Omicron BA.1 (A) Experimental schema (Created with BioRender.com ). (B) Histogram of CFSE cell trace expression by T cells after 7 days of co-culture, as well as CD45RA expression in CFSE negative and positive population (C). Representative plots of CD3 + CD4 + CD25 + CD45RA − T cells (D). Quantification of CD3 + CD4 + CFSE − CD25 + CD45RA − T cells of allogenic co-culture (E). Geometric mean of fluorescence intensity for CD45RA, CD25, PD1 surface markers on T cells (F). IL-2, IL-13, GMCSF, IFN- γ , IL-10 and IL-5 cytokine secretion by T cells after 7 days of allogenic co-culture with pDC stimulated with Medium, R848, and Delta or BA.1 SARS-CoV-2 viral variants. n = 8 healthy donors from 5 independent experiments. ∗, p < 0.05; ∗∗, p < 0.01; Mann-Whitney test. Bars represent means ± SD.

Article Snippet: TLR7/TLR8 agonist R848 (Resiquimod) , InvivoGen , Ref. tlrl-r848-1.

Techniques: Expressing, Co-Culture Assay, Fluorescence, MANN-WHITNEY

Stronger expression of co-stimulatory and migration markers in pDC following Omicron BA.1 exposure (A) Geometric mean of fluorescence intensity for PD-L1, CD80, CD86, and CCR7 surface markers on pDC stimulated by Medium, B220, Delta, or BA.1 with MOI = 0.4 or 4, for 20 h, n = 5. (B) Representative flow cytometry plots of CD80/CD86 expression on pDC upon Medium, R848 and SARS-CoV-2 variants stimulation. (C) % of CD86+CCR7+ cells upon SARS-CoV-2 variants stimulation . (D) % of CD80 + /CD86 + pDC cells co-cultured with 3%, 10%, 25%, and 45% of infected Vero cells by SARS-CoV-2 variants. (E) % of CD86+CCR7+ cells upon pDC stimulated with SARS COV2 variants at two doses of virus. (F) Heatmap of HLA-DR, PD-L1, CCR7, CD80, and CD86 expression in pDC SARS-CoV-2 activates samples (unsupervised FlowSom analysis, n = 8). ∗, p < 0.05; ∗∗, p < 0.01; A, D— Mann-Whitney test; C— two-way ANOVA test with Geisser-Greenhouse correction. Bars represent means ± SD.

Journal: iScience

Article Title: Differential response of human plasmacytoid pre-dendritic cells to SARS-CoV-2 variants

doi: 10.1016/j.isci.2025.113394

Figure Lengend Snippet: Stronger expression of co-stimulatory and migration markers in pDC following Omicron BA.1 exposure (A) Geometric mean of fluorescence intensity for PD-L1, CD80, CD86, and CCR7 surface markers on pDC stimulated by Medium, B220, Delta, or BA.1 with MOI = 0.4 or 4, for 20 h, n = 5. (B) Representative flow cytometry plots of CD80/CD86 expression on pDC upon Medium, R848 and SARS-CoV-2 variants stimulation. (C) % of CD86+CCR7+ cells upon SARS-CoV-2 variants stimulation . (D) % of CD80 + /CD86 + pDC cells co-cultured with 3%, 10%, 25%, and 45% of infected Vero cells by SARS-CoV-2 variants. (E) % of CD86+CCR7+ cells upon pDC stimulated with SARS COV2 variants at two doses of virus. (F) Heatmap of HLA-DR, PD-L1, CCR7, CD80, and CD86 expression in pDC SARS-CoV-2 activates samples (unsupervised FlowSom analysis, n = 8). ∗, p < 0.05; ∗∗, p < 0.01; A, D— Mann-Whitney test; C— two-way ANOVA test with Geisser-Greenhouse correction. Bars represent means ± SD.

Article Snippet: TLR7/TLR8 agonist R848 (Resiquimod) , InvivoGen , Ref. tlrl-r848-1.

Techniques: Expressing, Migration, Fluorescence, Flow Cytometry, Cell Culture, Infection, Virus, MANN-WHITNEY

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