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InvivoGen lipopolysaccharide lps
Lipopolysaccharide Lps, supplied by InvivoGen, used in various techniques. Bioz Stars score: 97/100, based on 1164 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 97 stars, based on 1164 article reviews

lipopolysaccharide lps - by Bioz Stars, 2026-05

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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: Lipopolysaccharide (LPS; Escherichia coli -derived, serotype O111:B4) was from List Biological Laboratories, Campbell, CA or Sigma-Aldrich Canada Co., Oakville, ON, and recombinant mouse IFN-β1 (carrier-free) was from Biolegend (San Diego, CA).

Techniques: Enzyme-linked Immunosorbent Assay, Control, Comparison

Induction of SLE autoantibodies with LPS is dependent on TRIF and partially dependent on MyD88. WT, MyD88 −/− , or TRIF −/− mice were immunized with β2GPI and LPS; all mice received four immunizations. Serum autoantibodies were detected by ELISA. Bars indicate the mean value±S.E. per group (n = 5–6 mice/group/experiment), and dots indicate values for individual mice. Data are pooled from two separate experiments. 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, mouse strains were compared by 2-way ANOVA, followed by a Dunnett's multiple comparison test. ∗∗∗∗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 with LPS is dependent on TRIF and partially dependent on MyD88. WT, MyD88 −/− , or TRIF −/− mice were immunized with β2GPI and LPS; all mice received four immunizations. Serum autoantibodies were detected by ELISA. Bars indicate the mean value±S.E. per group (n = 5–6 mice/group/experiment), and dots indicate values for individual mice. Data are pooled from two separate experiments. 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, mouse strains were compared by 2-way ANOVA, followed by a Dunnett's multiple comparison test. ∗∗∗∗P < 0.0001.

Techniques: Enzyme-linked Immunosorbent Assay, Comparison

Induction of SLE autoantibodies is diminished in the absence of IRF3 and IFNaR. WT, IRF3 −/− , or IFNaR −/− mice were immunized with β2GPI and LPS; all mice received four immunizations. Serum autoantibodies were detected by ELISA. Bars indicate the mean value±S.E. per group (n = 5–6 mice/group/experiment), and dots indicate values for individual mice. Data are pooled from two separate experiments. 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, anti-Sm, and anti-Sm/RNP) were analyzed statistically in separate groupings. For each of the two autoantibody categories, mouse strains were compared by 2-way ANOVA, followed by a Tukey's multiple comparison test. ∗∗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 is diminished in the absence of IRF3 and IFNaR. WT, IRF3 −/− , or IFNaR −/− mice were immunized with β2GPI and LPS; all mice received four immunizations. Serum autoantibodies were detected by ELISA. Bars indicate the mean value±S.E. per group (n = 5–6 mice/group/experiment), and dots indicate values for individual mice. Data are pooled from two separate experiments. 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, anti-Sm, and anti-Sm/RNP) were analyzed statistically in separate groupings. For each of the two autoantibody categories, mouse strains were compared by 2-way ANOVA, followed by a Tukey's multiple comparison test. ∗∗P < 0.01, ∗∗∗P < 0.001, and ∗∗∗∗P < 0.0001.

Techniques: Enzyme-linked Immunosorbent Assay, Comparison

Induction of hallmark SLE autoantibodies with LPS is enhanced in the presence of IFN-β in WT and TRIF-deficient, but not IRF3-deficient, mice. WT (A,B), TRIF −/− (C,D), and IRF3 −/− (E,F) mice were treated with IFN-β at the time of immunization with β2GPI and LPS and for two days after this immunization. All mice received five immunizations. Serum autoantibodies were detected by ELISA. Bars indicate the mean value±S.E. per group (n = 5 mice/group), and dots indicate values for individual mice. The OD 405 + 3 S.D. for unimmunized mice was ≤0.1 for all autoantibodies assayed. (A, C, E) Anti-β2GPI and anti-CL antibodies, and (B,D,F) hallmark SLE autoantibodies (anti-DNA, anti-Ro/SS-A, anti-La/SS-B, anti-Sm, and anti-Sm/RNP) were analyzed statistically in separate groupings. For each of the two autoantibody categories, mouse strains were compared by 2-way ANOVA, followed by a Tukey's multiple comparison test. ∗P < 0.05. ns = not significant.

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 hallmark SLE autoantibodies with LPS is enhanced in the presence of IFN-β in WT and TRIF-deficient, but not IRF3-deficient, mice. WT (A,B), TRIF −/− (C,D), and IRF3 −/− (E,F) mice were treated with IFN-β at the time of immunization with β2GPI and LPS and for two days after this immunization. All mice received five immunizations. Serum autoantibodies were detected by ELISA. Bars indicate the mean value±S.E. per group (n = 5 mice/group), and dots indicate values for individual mice. The OD 405 + 3 S.D. for unimmunized mice was ≤0.1 for all autoantibodies assayed. (A, C, E) Anti-β2GPI and anti-CL antibodies, and (B,D,F) hallmark SLE autoantibodies (anti-DNA, anti-Ro/SS-A, anti-La/SS-B, anti-Sm, and anti-Sm/RNP) were analyzed statistically in separate groupings. For each of the two autoantibody categories, mouse strains were compared by 2-way ANOVA, followed by a Tukey's multiple comparison test. ∗P < 0.05. ns = not significant.

Techniques: Enzyme-linked Immunosorbent Assay, Comparison

Immunization with β2GPI + LPS induces cell cycle and interferon signaling pathways in dendritic cells (DCs). (A) Heatmap of normalized gene expression (transcripts per million [TPM]) of selected genes in DCs for all experimental samples. Genes included in the heatmap are the top 20 differentially expressed genes between β2GPI/LPS-immunized WT mice (n = 3) and each experimental group (WT [PBS-immunized, n = 3]; and β2GPI/LPS-immunized TRIF −/− [n = 4], IRF3 −/− [n = 5], and IFNaR −/− [n = 5] mice). (B) Volcano plot of differential gene expression by splenic DCs from β2GPI/LPS-immunized and PBS-immunized WT mice. (C–D) Bar plot (C) and normalized enrichment score plots (D) of selected enriched pathways (p < 0.05) determined by gene set enrichment analysis (GSEA) for genes differentially expressed by DCs from β2GPI/LPS-immunized versus PBS-immunized WT mice. GSEA was performed using the REACTOME database. All cell cycle-related pathways were combined and analyzed as a single composite enrichment score. (E) Immune response enrichment analysis (IREA) of genes upregulated in β2GPI + LPS-immunized, compared to PBS-immunized WT mice. Significantly enriched IFN-I-related cytokines are highlighted in yellow and IFN-II-related cytokines are highlighted in green. Statistical significance was determined by two-sided Wilcoxon rank-sum test, followed by the Benjamini-Hochberg correction for multiple comparisons. The top 10 enriched cytokine signatures are shown. The minimal threshold for significance is p < 0.05.

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: Immunization with β2GPI + LPS induces cell cycle and interferon signaling pathways in dendritic cells (DCs). (A) Heatmap of normalized gene expression (transcripts per million [TPM]) of selected genes in DCs for all experimental samples. Genes included in the heatmap are the top 20 differentially expressed genes between β2GPI/LPS-immunized WT mice (n = 3) and each experimental group (WT [PBS-immunized, n = 3]; and β2GPI/LPS-immunized TRIF −/− [n = 4], IRF3 −/− [n = 5], and IFNaR −/− [n = 5] mice). (B) Volcano plot of differential gene expression by splenic DCs from β2GPI/LPS-immunized and PBS-immunized WT mice. (C–D) Bar plot (C) and normalized enrichment score plots (D) of selected enriched pathways (p < 0.05) determined by gene set enrichment analysis (GSEA) for genes differentially expressed by DCs from β2GPI/LPS-immunized versus PBS-immunized WT mice. GSEA was performed using the REACTOME database. All cell cycle-related pathways were combined and analyzed as a single composite enrichment score. (E) Immune response enrichment analysis (IREA) of genes upregulated in β2GPI + LPS-immunized, compared to PBS-immunized WT mice. Significantly enriched IFN-I-related cytokines are highlighted in yellow and IFN-II-related cytokines are highlighted in green. Statistical significance was determined by two-sided Wilcoxon rank-sum test, followed by the Benjamini-Hochberg correction for multiple comparisons. The top 10 enriched cytokine signatures are shown. The minimal threshold for significance is p < 0.05.

Techniques: Protein-Protein interactions, Gene Expression

Immunization with β2GPI + LPS induces cell cycle and interferon signalling pathways in macrophages. (A) Heatmap of normalized gene expression (transcripts per million [TPM]) of selected genes in macrophages for all experimental samples. Genes included in the heatmap are the top 20 differentially expressed genes between β2GPI/LPS-immunized WT mice (n = 3) and each experimental group (WT [PBS-immunized, n = 3]; and β2GPI/LPS-immunized TRIF −/− [n = 4], IRF3 −/− [n = 5], and IFNaR −/− [n = 5] mice). (B) Volcano plot of differential gene expression by splenic macrophages from β2GPI/LPS-immunized vs PBS-immunized WT mice. (C,D) Bar plot (C) and normalized enrichment score plots (D) of selected enriched pathways (p < 0.05) determined by gene set enrichment analysis (GSEA) for genes differentially expressed by macrophages from β2GPI/LPS-immunized vs PBS-immunized WT mice. GSEA was performed using the REACTOME database. All cell cycle-related pathways were combined and analyzed as a single composite enrichment score. (E) Immune response enrichment analysis (IREA) of genes upregulated in β2GPI + LPS-immunized, compared to PBS-immunized WT mice. Significantly enriched IFN-I-related cytokines are highlighted in yellow, IFN-II-related cytokines are highlighted in green, and NF-κB-dependent pro-inflammatory cytokines are highlighted in pink. Statistical significance was determined by two-sided Wilcoxon rank-sum test, followed by the Benjamini-Hochberg correction for multiple comparisons. The top 10 enriched cytokine signatures are shown. The minimal threshold for significance is p < 0.05.

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: Immunization with β2GPI + LPS induces cell cycle and interferon signalling pathways in macrophages. (A) Heatmap of normalized gene expression (transcripts per million [TPM]) of selected genes in macrophages for all experimental samples. Genes included in the heatmap are the top 20 differentially expressed genes between β2GPI/LPS-immunized WT mice (n = 3) and each experimental group (WT [PBS-immunized, n = 3]; and β2GPI/LPS-immunized TRIF −/− [n = 4], IRF3 −/− [n = 5], and IFNaR −/− [n = 5] mice). (B) Volcano plot of differential gene expression by splenic macrophages from β2GPI/LPS-immunized vs PBS-immunized WT mice. (C,D) Bar plot (C) and normalized enrichment score plots (D) of selected enriched pathways (p < 0.05) determined by gene set enrichment analysis (GSEA) for genes differentially expressed by macrophages from β2GPI/LPS-immunized vs PBS-immunized WT mice. GSEA was performed using the REACTOME database. All cell cycle-related pathways were combined and analyzed as a single composite enrichment score. (E) Immune response enrichment analysis (IREA) of genes upregulated in β2GPI + LPS-immunized, compared to PBS-immunized WT mice. Significantly enriched IFN-I-related cytokines are highlighted in yellow, IFN-II-related cytokines are highlighted in green, and NF-κB-dependent pro-inflammatory cytokines are highlighted in pink. Statistical significance was determined by two-sided Wilcoxon rank-sum test, followed by the Benjamini-Hochberg correction for multiple comparisons. The top 10 enriched cytokine signatures are shown. The minimal threshold for significance is p < 0.05.

Techniques: Gene Expression

TRIF- and IRF3-dependent genes upregulated in dendritic cells (DCs) following β2GPI/LPS-immunization are mostly IFN-I dependent. Genes upregulated in β2GPI/LPS-immunized WT (n = 3) vs PBS-immunized WT (n = 3) DCs were selected for downstream pathway analysis. (A) Venn diagram of the gene overlap between TRIF-dependent (upregulated in β2GPI/LPS-immunized WT vs TRIF −/− ; orange) and IRF3-dependent (upregulated in β2GPI/LPS-immunized WT vs IRF3 −/− ; green) genes. Genes that were both TRIF-and IRF3-dependent (blue circle) were selected for further analysis. (B,C) Pathway enrichment analysis of the 295 TRIF- and IRF3-dependent genes, using the PANTHER Gene Ontology: Biological Processes (B) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways databases (C). The top 10 differentially expressed pathways are shown for each analysis. (D) Immune responses enrichment analysis of the 295 TRIF- and IRF3-dependent genes. Significantly enriched IFN-I-related cytokines are highlighted in yellow and IFN-II-related cytokines are highlighted in green. Statistical significance was determined by two-sided Wilcoxon rank-sum test, followed by the Benjamini-Hochberg correction for multiple comparisons. The minimal threshold for significance is p < 0.05. (E) Volcano plot of differential gene expression for the 295 TRIF-and IRF3-dependent genes in β2GPI/LPS-immunized WT vs IFNaR −/− mice.

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: TRIF- and IRF3-dependent genes upregulated in dendritic cells (DCs) following β2GPI/LPS-immunization are mostly IFN-I dependent. Genes upregulated in β2GPI/LPS-immunized WT (n = 3) vs PBS-immunized WT (n = 3) DCs were selected for downstream pathway analysis. (A) Venn diagram of the gene overlap between TRIF-dependent (upregulated in β2GPI/LPS-immunized WT vs TRIF −/− ; orange) and IRF3-dependent (upregulated in β2GPI/LPS-immunized WT vs IRF3 −/− ; green) genes. Genes that were both TRIF-and IRF3-dependent (blue circle) were selected for further analysis. (B,C) Pathway enrichment analysis of the 295 TRIF- and IRF3-dependent genes, using the PANTHER Gene Ontology: Biological Processes (B) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways databases (C). The top 10 differentially expressed pathways are shown for each analysis. (D) Immune responses enrichment analysis of the 295 TRIF- and IRF3-dependent genes. Significantly enriched IFN-I-related cytokines are highlighted in yellow and IFN-II-related cytokines are highlighted in green. Statistical significance was determined by two-sided Wilcoxon rank-sum test, followed by the Benjamini-Hochberg correction for multiple comparisons. The minimal threshold for significance is p < 0.05. (E) Volcano plot of differential gene expression for the 295 TRIF-and IRF3-dependent genes in β2GPI/LPS-immunized WT vs IFNaR −/− mice.

Techniques: Gene Expression

TRIF- and IRF3-dependent genes upregulated in macrophages following β2GPI/LPS-immunization are mostly IFN-I-dependent. Genes upregulated in β2GPI/LPS-immunized WT (n = 3) vs PBS-immunized WT (n = 3) macrophages were selected for downstream pathway analysis. (A) Venn diagram of the gene overlap between TRIF-dependent (upregulated in β2GPI/LPS-immunized WT vs TRIF −/− ; orange) and IRF3-dependent (upregulated in β2GPI/LPS-immunized WT vs IRF3 −/− ; green) genes. Genes that were both TRIF- and IRF3-dependent (blue circle) were selected for further analysis. (B,C) Pathway enrichment analysis of the 154 TRIF- and IRF3-dependent genes, using the PANTHER Gene Ontology: Biological Processes (B) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways databases (C). The top 10 differentially expressed pathways are shown for each analysis. (D) Immune responses enrichment analysis of the 154 TRIF- and IRF3-dependent genes. Significantly enriched IFN-I-related cytokines are highlighted in yellow and IFN-II-related cytokines and highlighted in green. Statistical significance was determined by two-sided Wilcoxon rank-sum test, followed by the Benjamini-Hochberg correction for multiple comparisons. The top 10 enriched cytokine signatures are shown. The minimal threshold for significance is p < 0.05. (E) Volcano plot of differential gene expression for the 154 TRIF-and IRF3-dependent genes in β2GPI/LPS-immunized WT vs IFNaR −/− mice.

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: TRIF- and IRF3-dependent genes upregulated in macrophages following β2GPI/LPS-immunization are mostly IFN-I-dependent. Genes upregulated in β2GPI/LPS-immunized WT (n = 3) vs PBS-immunized WT (n = 3) macrophages were selected for downstream pathway analysis. (A) Venn diagram of the gene overlap between TRIF-dependent (upregulated in β2GPI/LPS-immunized WT vs TRIF −/− ; orange) and IRF3-dependent (upregulated in β2GPI/LPS-immunized WT vs IRF3 −/− ; green) genes. Genes that were both TRIF- and IRF3-dependent (blue circle) were selected for further analysis. (B,C) Pathway enrichment analysis of the 154 TRIF- and IRF3-dependent genes, using the PANTHER Gene Ontology: Biological Processes (B) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways databases (C). The top 10 differentially expressed pathways are shown for each analysis. (D) Immune responses enrichment analysis of the 154 TRIF- and IRF3-dependent genes. Significantly enriched IFN-I-related cytokines are highlighted in yellow and IFN-II-related cytokines and highlighted in green. Statistical significance was determined by two-sided Wilcoxon rank-sum test, followed by the Benjamini-Hochberg correction for multiple comparisons. The top 10 enriched cytokine signatures are shown. The minimal threshold for significance is p < 0.05. (E) Volcano plot of differential gene expression for the 154 TRIF-and IRF3-dependent genes in β2GPI/LPS-immunized WT vs IFNaR −/− mice.

Techniques: Gene Expression

TRIF- and IRF3-dependent genes with little to no IFNaR-dependence are associated with TNF production and signalling. (A) Venn diagram of the gene overlap between TRIF-dependent (upregulated in β2GPI/LPS-immunized WT vs TRIF −/− ; orange), IRF3-dependent (upregulated in β2GPI/LPS-immunized WT vs IRF3 −/− ; green), and IFNaR-dependent (upregulated in β2GPI/LPS-immunized WT vs IFNaR −/− ; yellow) genes in DCs. The 77 TRIF- and IRF3-dependent genes with little to no IFNaR-dependence (blue circle) were selected for further analysis. (B,C) Pathway enrichment analysis of the 77 TRIF- and IRF3-dependent genes with little to no IFNaR-dependency, using the PANTHER Gene Ontology: Biological Processes (B) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways databases (C). The top 10 differentially expressed pathways are shown for each analysis. (D) Immune response enrichment analysis of the of the 77 TRIF- and IRF3-dependent genes with little to no IFNaR-dependency. The significantly enriched NF-κB-dependent pro-inflammatory cytokine is highlighted in pink. Statistical significance was determined by two-sided Wilcoxon rank-sum test, followed by the Benjamini-Hochberg correction for multiple comparisons. The minimal threshold for significance is p < 0.05. (E) Venn diagram of the gene overlap between TRIF-dependent (upregulated in β2GPI/LPS-immunized WT vs TRIF −/− ; orange), IRF3-dependent (upregulated in β2GPI/LPS-immunized WT vs IRF3 −/− ; green), and IFNaR-dependent (upregulated in β2GPI/LPS-immunized WT vs IFNaR −/− ; yellow) genes in macrophages. The 6 TRIF- and IRF3-dependent genes with little to no IFNaR-dependence (blue circle) were selected for further analysis. (F) Transcript per million (TPM) of Tnf in macrophages for each experimental group. Data represent the mean ± SD. Statistical significance was determined by one-way ANOVA, followed by a Dunnett's post-hoc test. (G) C57BL/6 WT mice were injected intraperitoneally with β2GPI + PBS or β2GPI + LPS. TNF concentration was assayed in the serum by cytokine array assay (44-plex cytokine assay, Eve Technologies). Statistical significance was determined by Student's t-test. ns = not significant. ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001.

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: TRIF- and IRF3-dependent genes with little to no IFNaR-dependence are associated with TNF production and signalling. (A) Venn diagram of the gene overlap between TRIF-dependent (upregulated in β2GPI/LPS-immunized WT vs TRIF −/− ; orange), IRF3-dependent (upregulated in β2GPI/LPS-immunized WT vs IRF3 −/− ; green), and IFNaR-dependent (upregulated in β2GPI/LPS-immunized WT vs IFNaR −/− ; yellow) genes in DCs. The 77 TRIF- and IRF3-dependent genes with little to no IFNaR-dependence (blue circle) were selected for further analysis. (B,C) Pathway enrichment analysis of the 77 TRIF- and IRF3-dependent genes with little to no IFNaR-dependency, using the PANTHER Gene Ontology: Biological Processes (B) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways databases (C). The top 10 differentially expressed pathways are shown for each analysis. (D) Immune response enrichment analysis of the of the 77 TRIF- and IRF3-dependent genes with little to no IFNaR-dependency. The significantly enriched NF-κB-dependent pro-inflammatory cytokine is highlighted in pink. Statistical significance was determined by two-sided Wilcoxon rank-sum test, followed by the Benjamini-Hochberg correction for multiple comparisons. The minimal threshold for significance is p < 0.05. (E) Venn diagram of the gene overlap between TRIF-dependent (upregulated in β2GPI/LPS-immunized WT vs TRIF −/− ; orange), IRF3-dependent (upregulated in β2GPI/LPS-immunized WT vs IRF3 −/− ; green), and IFNaR-dependent (upregulated in β2GPI/LPS-immunized WT vs IFNaR −/− ; yellow) genes in macrophages. The 6 TRIF- and IRF3-dependent genes with little to no IFNaR-dependence (blue circle) were selected for further analysis. (F) Transcript per million (TPM) of Tnf in macrophages for each experimental group. Data represent the mean ± SD. Statistical significance was determined by one-way ANOVA, followed by a Dunnett's post-hoc test. (G) C57BL/6 WT mice were injected intraperitoneally with β2GPI + PBS or β2GPI + LPS. TNF concentration was assayed in the serum by cytokine array assay (44-plex cytokine assay, Eve Technologies). Statistical significance was determined by Student's t-test. ns = not significant. ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001.

Techniques: Injection, Concentration Assay, Cytokine Assay

TRIF- and IRF3-dependent genes from both DCs and macrophages have an SLE-like signature. (A) Venn diagram of the overlap of upregulated TRIF-dependent (upregulated in β2GPI/LPS-immunized WT vs TRIF −/− ) and IRF3-dependent (upregulated in β2GPI/LPS-immunized WT vs IRF3 −/− ) genes between DCs (blue) and macrophages (red). The TRIF-and IRF3-dependent genes that were upregulated in both DCs and macrophages were selected for further analysis. (B,C) Pathway enrichment analysis of the 27 TRIF- and IRF3-dependent genes upregulated in both DCs and macrophages, using the PANTHER Gene Ontology: Biological Processes (B) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways databases (C). The top 10 differentially expressed pathways are shown for each analysis. (D) Immune responses enrichment analysis of the 27 TRIF- and IRF3-dependent genes upregulated in both DCs and macrophages. Significantly enriched IFN-I-related cytokines are highlighted in yellow and IFN-II-related cytokines are highlighted in green. Statistical significance was determined by two-sided Wilcoxon rank-sum test, followed by the Benjamini-Hochberg correction for multiple comparisons. The top 10 enriched cytokine signatures are shown. The minimal threshold for significance is p < 0.05. (E) Transcription factor enrichment analysis of the 27 TRIF- and IRF3-dependent genes upregulated in both DCs and macrophages. The top 10 transcription factors associated with this gene signature are included. Distance between transcription factors was adjusted for readability. (F) Disease signature enrichment analysis of the 27 TRIF- and IRF3-dependent genes upregulated in both DCs and macrophages. The top 10 enriched disease signatures from DiSignAtlas are included. The DiSignAtlas ID of the top 10 enriched disease signatures are as follows: DSA02284, DSA01156, DSA03951, DSA02253, DSA07100, DSA04468, DSA01254, DSA01302, DSA08191, and DSA03028.

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: TRIF- and IRF3-dependent genes from both DCs and macrophages have an SLE-like signature. (A) Venn diagram of the overlap of upregulated TRIF-dependent (upregulated in β2GPI/LPS-immunized WT vs TRIF −/− ) and IRF3-dependent (upregulated in β2GPI/LPS-immunized WT vs IRF3 −/− ) genes between DCs (blue) and macrophages (red). The TRIF-and IRF3-dependent genes that were upregulated in both DCs and macrophages were selected for further analysis. (B,C) Pathway enrichment analysis of the 27 TRIF- and IRF3-dependent genes upregulated in both DCs and macrophages, using the PANTHER Gene Ontology: Biological Processes (B) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways databases (C). The top 10 differentially expressed pathways are shown for each analysis. (D) Immune responses enrichment analysis of the 27 TRIF- and IRF3-dependent genes upregulated in both DCs and macrophages. Significantly enriched IFN-I-related cytokines are highlighted in yellow and IFN-II-related cytokines are highlighted in green. Statistical significance was determined by two-sided Wilcoxon rank-sum test, followed by the Benjamini-Hochberg correction for multiple comparisons. The top 10 enriched cytokine signatures are shown. The minimal threshold for significance is p < 0.05. (E) Transcription factor enrichment analysis of the 27 TRIF- and IRF3-dependent genes upregulated in both DCs and macrophages. The top 10 transcription factors associated with this gene signature are included. Distance between transcription factors was adjusted for readability. (F) Disease signature enrichment analysis of the 27 TRIF- and IRF3-dependent genes upregulated in both DCs and macrophages. The top 10 enriched disease signatures from DiSignAtlas are included. The DiSignAtlas ID of the top 10 enriched disease signatures are as follows: DSA02284, DSA01156, DSA03951, DSA02253, DSA07100, DSA04468, DSA01254, DSA01302, DSA08191, and DSA03028.

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