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imiquimod  (InvivoGen)


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    Structured Review

    InvivoGen imiquimod
    DCIR suppresses TLR7-mediated signaling (A–D) Cytokine production from GMDCs upon stimulation with <t>imiquimod,</t> a TLR7 agonist. GMDCs were stimulated with imiquimod (1 μg/mL) for 3 days, and the amount of cytokine was determined using an ELISA assay. The concentration of cytokine was determined with ELISA (A; IL-1β, B; IL-6, C; p40, D; TNF-α). The bars show mean ± SD of triplicate wells and the data are representative of two independent experiments. ∗∗, p < 0.01, ∗, p < 0.05. (E) Spleen images of WT and Dcir −/− mice after i.v. injection of IMQ. Spleens were removed 24 h after IMQ i.v. injection. (F and G) Spleen weight (F) and splenocyte cell numbers (G). PBS-injected WT mice; solid circles, IMW-injected WT mice; dark gray circles, PBS-injected Dcir −/− mice; open circles, IMQ-injected Dcir −/− mice; light gray circles. Each symbol shows an individual mouse and a horizontal bar represents the mean for each score. Statistical significances were evaluated using one-way ANOVA with Tukey’s post hoc test (∗∗, p < 0.01, ∗, p < 0.05). The data are representative of two independent experiments (E–G). (H) Spontaneous EAE-like encephalomyelitis symptoms in 2D2Tg Dcir −/− Tlr7 −/− mice. 2D2Tg mice ( n = 37) and 2D2Tg Dcir −/− Tlr7 −/− mice ( n = 24) were monitored for 60 weeks 2D2Tg mice (sky blue) and 2D2Tg Dcir −/− Tlr7 −/− mice (red). (I) Disease severity of spontaneous development of EAE-like encephalomyelitis symptoms in 2D2Tg mice (sky blue) and 2D2Tg Dcir −/− Tlr7 −/− mice (red). (J) PTX administration into 2D2Tg mice and 2D2Tg Dcir −/− Tlr7 −/− mice. 2D2Tg mice ( n = 10) and 2D2Tg Dcir −/− Tlr7 −/− mice ( n = 8) were administered pTx twice, at day 0 and day 2, and monitored for 30 days. Statistical significance was evaluated using the Mann-Whitney U test. (K) Incidence of EAE-like encephalomyelitis after PTX administration in 2D2Tg mice (sky blue) and 2D2Tg Dcir −/− Tlr7 −/− mice (red). The data were representative of two independent experiments.
    Imiquimod, supplied by InvivoGen, used in various techniques. Bioz Stars score: 96/100, based on 1054 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "DCIR-mediated inhibitory regulation of TLR7-MyD88 axis prevents autoimmune neuroinflammation"

    Article Title: DCIR-mediated inhibitory regulation of TLR7-MyD88 axis prevents autoimmune neuroinflammation

    Journal: iScience

    doi: 10.1016/j.isci.2026.116094

    DCIR suppresses TLR7-mediated signaling (A–D) Cytokine production from GMDCs upon stimulation with imiquimod, a TLR7 agonist. GMDCs were stimulated with imiquimod (1 μg/mL) for 3 days, and the amount of cytokine was determined using an ELISA assay. The concentration of cytokine was determined with ELISA (A; IL-1β, B; IL-6, C; p40, D; TNF-α). The bars show mean ± SD of triplicate wells and the data are representative of two independent experiments. ∗∗, p < 0.01, ∗, p < 0.05. (E) Spleen images of WT and Dcir −/− mice after i.v. injection of IMQ. Spleens were removed 24 h after IMQ i.v. injection. (F and G) Spleen weight (F) and splenocyte cell numbers (G). PBS-injected WT mice; solid circles, IMW-injected WT mice; dark gray circles, PBS-injected Dcir −/− mice; open circles, IMQ-injected Dcir −/− mice; light gray circles. Each symbol shows an individual mouse and a horizontal bar represents the mean for each score. Statistical significances were evaluated using one-way ANOVA with Tukey’s post hoc test (∗∗, p < 0.01, ∗, p < 0.05). The data are representative of two independent experiments (E–G). (H) Spontaneous EAE-like encephalomyelitis symptoms in 2D2Tg Dcir −/− Tlr7 −/− mice. 2D2Tg mice ( n = 37) and 2D2Tg Dcir −/− Tlr7 −/− mice ( n = 24) were monitored for 60 weeks 2D2Tg mice (sky blue) and 2D2Tg Dcir −/− Tlr7 −/− mice (red). (I) Disease severity of spontaneous development of EAE-like encephalomyelitis symptoms in 2D2Tg mice (sky blue) and 2D2Tg Dcir −/− Tlr7 −/− mice (red). (J) PTX administration into 2D2Tg mice and 2D2Tg Dcir −/− Tlr7 −/− mice. 2D2Tg mice ( n = 10) and 2D2Tg Dcir −/− Tlr7 −/− mice ( n = 8) were administered pTx twice, at day 0 and day 2, and monitored for 30 days. Statistical significance was evaluated using the Mann-Whitney U test. (K) Incidence of EAE-like encephalomyelitis after PTX administration in 2D2Tg mice (sky blue) and 2D2Tg Dcir −/− Tlr7 −/− mice (red). The data were representative of two independent experiments.
    Figure Legend Snippet: DCIR suppresses TLR7-mediated signaling (A–D) Cytokine production from GMDCs upon stimulation with imiquimod, a TLR7 agonist. GMDCs were stimulated with imiquimod (1 μg/mL) for 3 days, and the amount of cytokine was determined using an ELISA assay. The concentration of cytokine was determined with ELISA (A; IL-1β, B; IL-6, C; p40, D; TNF-α). The bars show mean ± SD of triplicate wells and the data are representative of two independent experiments. ∗∗, p < 0.01, ∗, p < 0.05. (E) Spleen images of WT and Dcir −/− mice after i.v. injection of IMQ. Spleens were removed 24 h after IMQ i.v. injection. (F and G) Spleen weight (F) and splenocyte cell numbers (G). PBS-injected WT mice; solid circles, IMW-injected WT mice; dark gray circles, PBS-injected Dcir −/− mice; open circles, IMQ-injected Dcir −/− mice; light gray circles. Each symbol shows an individual mouse and a horizontal bar represents the mean for each score. Statistical significances were evaluated using one-way ANOVA with Tukey’s post hoc test (∗∗, p < 0.01, ∗, p < 0.05). The data are representative of two independent experiments (E–G). (H) Spontaneous EAE-like encephalomyelitis symptoms in 2D2Tg Dcir −/− Tlr7 −/− mice. 2D2Tg mice ( n = 37) and 2D2Tg Dcir −/− Tlr7 −/− mice ( n = 24) were monitored for 60 weeks 2D2Tg mice (sky blue) and 2D2Tg Dcir −/− Tlr7 −/− mice (red). (I) Disease severity of spontaneous development of EAE-like encephalomyelitis symptoms in 2D2Tg mice (sky blue) and 2D2Tg Dcir −/− Tlr7 −/− mice (red). (J) PTX administration into 2D2Tg mice and 2D2Tg Dcir −/− Tlr7 −/− mice. 2D2Tg mice ( n = 10) and 2D2Tg Dcir −/− Tlr7 −/− mice ( n = 8) were administered pTx twice, at day 0 and day 2, and monitored for 30 days. Statistical significance was evaluated using the Mann-Whitney U test. (K) Incidence of EAE-like encephalomyelitis after PTX administration in 2D2Tg mice (sky blue) and 2D2Tg Dcir −/− Tlr7 −/− mice (red). The data were representative of two independent experiments.

    Techniques Used: Enzyme-linked Immunosorbent Assay, Concentration Assay, Injection, MANN-WHITNEY



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    Image Search Results


    DCIR suppresses TLR7-mediated signaling (A–D) Cytokine production from GMDCs upon stimulation with imiquimod, a TLR7 agonist. GMDCs were stimulated with imiquimod (1 μg/mL) for 3 days, and the amount of cytokine was determined using an ELISA assay. The concentration of cytokine was determined with ELISA (A; IL-1β, B; IL-6, C; p40, D; TNF-α). The bars show mean ± SD of triplicate wells and the data are representative of two independent experiments. ∗∗, p < 0.01, ∗, p < 0.05. (E) Spleen images of WT and Dcir −/− mice after i.v. injection of IMQ. Spleens were removed 24 h after IMQ i.v. injection. (F and G) Spleen weight (F) and splenocyte cell numbers (G). PBS-injected WT mice; solid circles, IMW-injected WT mice; dark gray circles, PBS-injected Dcir −/− mice; open circles, IMQ-injected Dcir −/− mice; light gray circles. Each symbol shows an individual mouse and a horizontal bar represents the mean for each score. Statistical significances were evaluated using one-way ANOVA with Tukey’s post hoc test (∗∗, p < 0.01, ∗, p < 0.05). The data are representative of two independent experiments (E–G). (H) Spontaneous EAE-like encephalomyelitis symptoms in 2D2Tg Dcir −/− Tlr7 −/− mice. 2D2Tg mice ( n = 37) and 2D2Tg Dcir −/− Tlr7 −/− mice ( n = 24) were monitored for 60 weeks 2D2Tg mice (sky blue) and 2D2Tg Dcir −/− Tlr7 −/− mice (red). (I) Disease severity of spontaneous development of EAE-like encephalomyelitis symptoms in 2D2Tg mice (sky blue) and 2D2Tg Dcir −/− Tlr7 −/− mice (red). (J) PTX administration into 2D2Tg mice and 2D2Tg Dcir −/− Tlr7 −/− mice. 2D2Tg mice ( n = 10) and 2D2Tg Dcir −/− Tlr7 −/− mice ( n = 8) were administered pTx twice, at day 0 and day 2, and monitored for 30 days. Statistical significance was evaluated using the Mann-Whitney U test. (K) Incidence of EAE-like encephalomyelitis after PTX administration in 2D2Tg mice (sky blue) and 2D2Tg Dcir −/− Tlr7 −/− mice (red). The data were representative of two independent experiments.

    Journal: iScience

    Article Title: DCIR-mediated inhibitory regulation of TLR7-MyD88 axis prevents autoimmune neuroinflammation

    doi: 10.1016/j.isci.2026.116094

    Figure Lengend Snippet: DCIR suppresses TLR7-mediated signaling (A–D) Cytokine production from GMDCs upon stimulation with imiquimod, a TLR7 agonist. GMDCs were stimulated with imiquimod (1 μg/mL) for 3 days, and the amount of cytokine was determined using an ELISA assay. The concentration of cytokine was determined with ELISA (A; IL-1β, B; IL-6, C; p40, D; TNF-α). The bars show mean ± SD of triplicate wells and the data are representative of two independent experiments. ∗∗, p < 0.01, ∗, p < 0.05. (E) Spleen images of WT and Dcir −/− mice after i.v. injection of IMQ. Spleens were removed 24 h after IMQ i.v. injection. (F and G) Spleen weight (F) and splenocyte cell numbers (G). PBS-injected WT mice; solid circles, IMW-injected WT mice; dark gray circles, PBS-injected Dcir −/− mice; open circles, IMQ-injected Dcir −/− mice; light gray circles. Each symbol shows an individual mouse and a horizontal bar represents the mean for each score. Statistical significances were evaluated using one-way ANOVA with Tukey’s post hoc test (∗∗, p < 0.01, ∗, p < 0.05). The data are representative of two independent experiments (E–G). (H) Spontaneous EAE-like encephalomyelitis symptoms in 2D2Tg Dcir −/− Tlr7 −/− mice. 2D2Tg mice ( n = 37) and 2D2Tg Dcir −/− Tlr7 −/− mice ( n = 24) were monitored for 60 weeks 2D2Tg mice (sky blue) and 2D2Tg Dcir −/− Tlr7 −/− mice (red). (I) Disease severity of spontaneous development of EAE-like encephalomyelitis symptoms in 2D2Tg mice (sky blue) and 2D2Tg Dcir −/− Tlr7 −/− mice (red). (J) PTX administration into 2D2Tg mice and 2D2Tg Dcir −/− Tlr7 −/− mice. 2D2Tg mice ( n = 10) and 2D2Tg Dcir −/− Tlr7 −/− mice ( n = 8) were administered pTx twice, at day 0 and day 2, and monitored for 30 days. Statistical significance was evaluated using the Mann-Whitney U test. (K) Incidence of EAE-like encephalomyelitis after PTX administration in 2D2Tg mice (sky blue) and 2D2Tg Dcir −/− Tlr7 −/− mice (red). The data were representative of two independent experiments.

    Article Snippet: Imiquimod , InvivoGen , #99011-78-6.

    Techniques: Enzyme-linked Immunosorbent Assay, Concentration Assay, Injection, MANN-WHITNEY

    Induction of SLE autoantibodies occurs in the presence of LPS or Poly I:C, but not other TLR ligands. Wild type (WT) C57BL/6 mice received five immunizations with β2GPI in combination with one of the following TLR ligands: TLR2 : PAM2, FSL-1 (lipoprotein); TLR3 : Poly I:C (dsRNA); TLR4 : LPS; TLR7: IMQ (imiquimod); or TLR9 : CpG-ODN (ssDNA). Serum autoantibodies were detected by ELISA. Bars indicate the mean value +/standard error (S.E.) per group (n = 5 mice/group), and dots indicate values for individual mice. Autoantibody levels for control mice immunized with PBS and TLR ligand were OD 405 < 0.1. The OD 405 + 3 S.D. for unimmunized mice was ≤0.1 for all autoantibodies assayed. (A) Anti-β2GPI and anti-CL antibodies, and (B) hallmark SLE autoantibodies (anti-DNA, anti-Ro/SS-A, anti-La/SS-B, and anti-Sm) were analyzed statistically in separate groupings. For each of the two autoantibody categories, each different TLR ligand (immunized with β2GPI) was compared to the other TLR ligands by 2-way ANOVA, followed by a Tukey's multiple comparison test. ns = not significant. ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001, and ∗∗∗∗P < 0.0001.

    Journal: Journal of Translational Autoimmunity

    Article Title: Type I interferon-dependent and -independent signaling underlie autoantibody production in a murine lupus model

    doi: 10.1016/j.jtauto.2026.100351

    Figure Lengend Snippet: Induction of SLE autoantibodies occurs in the presence of LPS or Poly I:C, but not other TLR ligands. Wild type (WT) C57BL/6 mice received five immunizations with β2GPI in combination with one of the following TLR ligands: TLR2 : PAM2, FSL-1 (lipoprotein); TLR3 : Poly I:C (dsRNA); TLR4 : LPS; TLR7: IMQ (imiquimod); or TLR9 : CpG-ODN (ssDNA). Serum autoantibodies were detected by ELISA. Bars indicate the mean value +/standard error (S.E.) per group (n = 5 mice/group), and dots indicate values for individual mice. Autoantibody levels for control mice immunized with PBS and TLR ligand were OD 405 < 0.1. The OD 405 + 3 S.D. for unimmunized mice was ≤0.1 for all autoantibodies assayed. (A) Anti-β2GPI and anti-CL antibodies, and (B) hallmark SLE autoantibodies (anti-DNA, anti-Ro/SS-A, anti-La/SS-B, and anti-Sm) were analyzed statistically in separate groupings. For each of the two autoantibody categories, each different TLR ligand (immunized with β2GPI) was compared to the other TLR ligands by 2-way ANOVA, followed by a Tukey's multiple comparison test. ns = not significant. ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001, and ∗∗∗∗P < 0.0001.

    Article Snippet: TLR ligands Pam2CSK4 (PAM2), FSL-1, Pam3CSK4 (PAM3), Poly I:C (HMW), imiquimod-R837 (IMQ), and CpG-ODN-1555 + 1466 (CpG-ODN) were from InvivoGen (San Diego, CA).

    Techniques: Enzyme-linked Immunosorbent Assay, Control, Comparison