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tlr ligands pam2csk4 pam2  (InvivoGen)


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    Structured Review

    InvivoGen tlr ligands pam2csk4 pam2
    Induction of SLE autoantibodies occurs in the presence of LPS or Poly I:C, but not other <t>TLR</t> <t>ligands.</t> Wild type (WT) C57BL/6 mice received five immunizations with β2GPI in combination with one of the following TLR ligands: TLR2 : <t>PAM2,</t> 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.
    Tlr Ligands Pam2csk4 Pam2, supplied by InvivoGen, used in various techniques. Bioz Stars score: 96/100, based on 564 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Type I interferon-dependent and -independent signaling underlie autoantibody production in a murine lupus model"

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

    Journal: Journal of Translational Autoimmunity

    doi: 10.1016/j.jtauto.2026.100351

    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.
    Figure Legend 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.

    Techniques Used: Enzyme-linked Immunosorbent Assay, Control, Comparison



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    Induction of SLE autoantibodies occurs in the presence of LPS or Poly I:C, but not other <t>TLR</t> <t>ligands.</t> Wild type (WT) C57BL/6 mice received five immunizations with β2GPI in combination with one of the following TLR ligands: TLR2 : <t>PAM2,</t> 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.
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    a , Integrative clustering of clinical, proteomic and metabolomic data using Fuzzy C-Means clustering across all time points. Normalized multi-omics revealed analytes that increased after xenotransplant despite the administered immunosuppressive regimen. b , Network analysis integrating proteomic and metabolomic data shows several modules enriched for innate immunity pathways. c , Experimental scheme showing that recipient PBMCs obtained at multiple time points were stimulated for 24 h with a regimen of <t>TLR</t> ligands (LPS, <t>Pam3CSK4,</t> <t>R848</t> and p:IC), following which cytokine concentrations were measured in supernatants using a Luminex device. d – g , Longitudinal concentrations of IL-1β ( d ), IL-6 ( e ), IL-8 ( f ) and GM-CSF ( g ) following TLR ligand stimulation.
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    Image Search Results


    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

    a , Integrative clustering of clinical, proteomic and metabolomic data using Fuzzy C-Means clustering across all time points. Normalized multi-omics revealed analytes that increased after xenotransplant despite the administered immunosuppressive regimen. b , Network analysis integrating proteomic and metabolomic data shows several modules enriched for innate immunity pathways. c , Experimental scheme showing that recipient PBMCs obtained at multiple time points were stimulated for 24 h with a regimen of TLR ligands (LPS, Pam3CSK4, R848 and p:IC), following which cytokine concentrations were measured in supernatants using a Luminex device. d – g , Longitudinal concentrations of IL-1β ( d ), IL-6 ( e ), IL-8 ( f ) and GM-CSF ( g ) following TLR ligand stimulation.

    Journal: Nature Medicine

    Article Title: Immune profiling in a living human recipient of a gene-edited pig kidney

    doi: 10.1038/s41591-025-04053-3

    Figure Lengend Snippet: a , Integrative clustering of clinical, proteomic and metabolomic data using Fuzzy C-Means clustering across all time points. Normalized multi-omics revealed analytes that increased after xenotransplant despite the administered immunosuppressive regimen. b , Network analysis integrating proteomic and metabolomic data shows several modules enriched for innate immunity pathways. c , Experimental scheme showing that recipient PBMCs obtained at multiple time points were stimulated for 24 h with a regimen of TLR ligands (LPS, Pam3CSK4, R848 and p:IC), following which cytokine concentrations were measured in supernatants using a Luminex device. d – g , Longitudinal concentrations of IL-1β ( d ), IL-6 ( e ), IL-8 ( f ) and GM-CSF ( g ) following TLR ligand stimulation.

    Article Snippet: Cells were stimulated with 100 μl of either complete RPMI (controls) or a mixture of bacterial and viral TLR ligands (0.025 μg ml −1 LPS, 10 μg ml −1 Pam3CSK4, 4 μg ml −1 R848, 25 μg ml −1 poly I:C—all from Invivogen).

    Techniques: Metabolomic, Biomarker Discovery, Luminex