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R&D Systems enzyme linked immunosorbent assay elisa kit
Enzyme Linked Immunosorbent Assay Elisa Kit, supplied by R&D Systems, used in various techniques. Bioz Stars score: 96/100, based on 195 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/cxcl10+duoset+elisa+kits/Mouse+CXCL10%2FIP-10%2FCRG-2+DuoSet+ELISA/pm42018138-109-20-25
Average 96 stars, based on 195 article reviews

enzyme linked immunosorbent assay elisa kit - by Bioz Stars, 2026-11

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Article Title: CXCL9 inhibits tumour growth and drives anti-PD-L1 therapy in ovarian cancer
Article Snippet: Antibodies were diluted in InVivo Pure pH 7.0 Dilution Buffer (Cat. #IP0070, Bio X Cell) and injected at 2 μg/μl dosage twice a week until endpoints were reached. .. Ascitic fluid was centrifugated and the supernatant was used in Cxcl9 and Cxcl10 DuoSet ELISA Kits from R&D Systems (Cat. #DY492 and #DY466). .. The resulting chemokine concentrations were normalised to total protein amounts of ascitic supernatants, determined by a Bradford assay with Coomassie Brilliant Blue G-250 (Cat. #27815, Sigma-Aldrich) and bovine serum albumin (Cat. #1470, Sigma-Aldrich).

Article Title: PINX1 and TERT Are Required for TNF-α-Induced Airway Smooth Muscle Chemokine Gene Expression.
Article Snippet: .. MST312 was purchased from Sigma-Aldrich, BIBR1532 was purchased from Tocris Biosciences, and CCL2, CCL5, CCL11, CXCL8, and CXCL10 DuoSet ELISA kits and recombinant human TNF-a were purchased from R&D Systems. .. TERT (SC-7212), PINX1 (SC-292115), p65 (Rel-A; SC372) and GAPDH (SC20357) Abs were purchased from Santa Cruz Biotechnology (Dallas, TX).

Article Title: CXCL9 inhibits tumour growth and drives anti-PD-L1 therapy in ovarian cancer.
Article Snippet: Antibodies were diluted in InVivoPure pH 7.0 Dilution Buffer (Cat. #IP0070, Bio X Cell) and injected at 2 μg/μl dosage twice a week until endpoints were reached. .. Evaluation of ascitic chemokine concentrations with ELISA Ascitic fluid was centrifugated and the supernatant was used in Cxcl9 and Cxcl10 DuoSet ELISA Kits from R&D Systems (Cat. #DY492 and #DY466). .. The resulting chemokine concentrations were normalised to total protein amounts of ascitic supernatants, determined by a Bradford assay with Coomassie Brilliant Blue G-250 (Cat. #27815, Sigma-Aldrich) and bovine serum albumin (Cat. #1470, Sigma-Aldrich).

Article Title: Type III interferon inhibits bladder cancer progression by reprogramming macrophage-mediated phagocytosis and orchestrating effective immune responses.
Article Snippet: The Mouse IFN-λ2/3 DuoSet ELISA Kits (R&D Systems, USA) were used to measure the expression of IFN-λ3 in mouse bladder tumor tissues or cell line supernatants (online supplemental table 6). .. In the case of human samples, the expression of CXCL9 and CXCL10 in Mφs, supernatants stimulated with human IFN-λ1 (10 ng/mL) or IFN-α (10 ng/mL) were quantified using the human CXCL9 and CXCL10 DuoSet ELISA Kits (R&D Systems, USA; online supplemental table 6). ..

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G9a inhibition potentiates the immunogenic effects of IFN-γ in HCC cells (A) Effect of CM272 and EZM8266 on IFN-γ-triggered CXCL10 production in murine (PM299L) and human (HuH7) HCC cells. Cells were treated with CM272 for 48 h or with CM272 for 24 h and then with IFN-γ (75 U/mL) for another 24 h or with IFN-γ alone for 24 h. PM299L were treated with 400 nM, and HuH7 received 1 μM of CM272 ( n = 3). For EZM8266, cells were pretreated for 48 h with EZM8266 (5 mM) and then with IFN-γ (75 U/mL) for another 24 h, as indicated. CXCL10 protein levels were measured by ELISA in cells’ conditioned media ( n = 3). (B) Effect of G9a inhibition with CM272 or EZM8266 on the expression of MHC class I complex protein (MHC-I) on the surface of PM299L cells. Cells were treated with IFN-γ and CM272 or EZM8266 as indicated in (A), and MHC-I levels were determined by FACS analysis ( n = 3). (C) ChIP analyses of H3K9me2 levels in the proximal promoter regions of CXCL10 and HLA-A genes in HuH7 cells treated with IFN-γ (75 U/mL) and CM272 (400 nM), as indicated in (A) ( n = 3). (D) Evaluation of the expression of transposable elements (TEs) and endogenous retroviral sequences (ERVs) by RNA-seq in NM53 murine HCC cells treated with IFN-γ, CM272, and their combination as indicated in (A). (E) Immunofluorescence analyses of dsRNA in PM299L HCC cells treated with CM272 (24 h) or EZM8266 (48 h). Representative images are shown. Scale bars, 10 μm. Right panel shows a control without primary antibody ( n = 3). Data are represented as mean ± SEM. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001. All the replicates represent biological replicates.

Journal: Cell Reports Medicine

Article Title: Histone methyl-transferase G9a inhibition boosts the efficacy of immune checkpoint inhibitors in experimental hepatocellular carcinoma

doi: 10.1016/j.xcrm.2026.102717

Figure Lengend Snippet: G9a inhibition potentiates the immunogenic effects of IFN-γ in HCC cells (A) Effect of CM272 and EZM8266 on IFN-γ-triggered CXCL10 production in murine (PM299L) and human (HuH7) HCC cells. Cells were treated with CM272 for 48 h or with CM272 for 24 h and then with IFN-γ (75 U/mL) for another 24 h or with IFN-γ alone for 24 h. PM299L were treated with 400 nM, and HuH7 received 1 μM of CM272 ( n = 3). For EZM8266, cells were pretreated for 48 h with EZM8266 (5 mM) and then with IFN-γ (75 U/mL) for another 24 h, as indicated. CXCL10 protein levels were measured by ELISA in cells’ conditioned media ( n = 3). (B) Effect of G9a inhibition with CM272 or EZM8266 on the expression of MHC class I complex protein (MHC-I) on the surface of PM299L cells. Cells were treated with IFN-γ and CM272 or EZM8266 as indicated in (A), and MHC-I levels were determined by FACS analysis ( n = 3). (C) ChIP analyses of H3K9me2 levels in the proximal promoter regions of CXCL10 and HLA-A genes in HuH7 cells treated with IFN-γ (75 U/mL) and CM272 (400 nM), as indicated in (A) ( n = 3). (D) Evaluation of the expression of transposable elements (TEs) and endogenous retroviral sequences (ERVs) by RNA-seq in NM53 murine HCC cells treated with IFN-γ, CM272, and their combination as indicated in (A). (E) Immunofluorescence analyses of dsRNA in PM299L HCC cells treated with CM272 (24 h) or EZM8266 (48 h). Representative images are shown. Scale bars, 10 μm. Right panel shows a control without primary antibody ( n = 3). Data are represented as mean ± SEM. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001. All the replicates represent biological replicates.

Article Snippet: CXCL9 and CXCL10 concentrations were measured in culture supernatants collected at the end of the incubation periods using commercial ELISA kits for mouse CXCL9 (DY492) and CXCL10 (DY466), both from R&D Systems, and an ELISA kit for human CXCL10 (550926) from BD Biosciences (Franklin Lanes, NJ, USA).

Techniques: Inhibition, Enzyme-linked Immunosorbent Assay, Expressing, Retroviral, RNA Sequencing, Immunofluorescence, Control

RRBP1 inhibition increases the CXCL10 mRNA stability in BC. ( A ) The volcano plot showed that differentially expressed genes regulated by RRBP1 inhibition in MB49 cells. ( B ) KEGG analysis for differentially expressed genes found enrichment signaling pathways in MB49 cells. ( C ) KEGG analysis for differentially expressed genes found enrichment signaling pathways in tumor samples. ( D, E ) Heatmap displays the expression changes of cytokines after RRBP1 inhibition in MB49 cells and tumor tissues. ( F ) The Venn diagram illustrates the differentially expressed cytokines in both MB49 cells and tumor tissues after inhibition of RRBP1. ( G ) Representative images of IHC staining for RRBP1 and CXCL10 expression in BC samples. ( H ) The correlation between RRBP1 expression and CXCL10 expression was analyzed based on 96 patients from in-house BC cohort. Scale bar: 50 µm. ( I ) The mRNA expression of CXCL10 after genetic or pharmacological inhibition of RRBP1 in T24. ( J ) ELISA analysis of CXCL10 expression after genetic or pharmacological inhibition of RRBP1 in T24. ( K ) Distribution of RRBP1-binding peaks across CXCL10 by integrative genomics Viewer. ( L, M ) RIP analyses of MB49 cells or T24 cells were performed with an anti-RRBP1 antibody followed by qPCR analyses with primer against CXCL10 mRNA. ( N, O ) Knockdown of ENO1 to detect the CXCL10 mRNA expression levels in MB49 cells or T24 cells that were treated with actinomycin D for the indicated time. Data are represented as mean means±SD. Statistical analysis was performed using unpaired two-tailed t-test ( I, J, L, M, N, O ) or Spearman correlation analysis ( H ). The data presented represent one or three independent experiments. *p<0.05, ***p<0.001. BC, bladder cancer; mRNA, messenger RNA; qPCR, quantitative PCR; RRB1, ribosomal-binding protein 1; IHC, immunohistochemistry; KEGG, Kyoto Encyclopedia of Genes and Genomes.

Journal: Journal for Immunotherapy of Cancer

Article Title: Targeting RRBP1 reverses immune evasion and enhances immunotherapy efficacy via the CXCL10-CXCR3 axis in bladder cancer

doi: 10.1136/jitc-2025-013809

Figure Lengend Snippet: RRBP1 inhibition increases the CXCL10 mRNA stability in BC. ( A ) The volcano plot showed that differentially expressed genes regulated by RRBP1 inhibition in MB49 cells. ( B ) KEGG analysis for differentially expressed genes found enrichment signaling pathways in MB49 cells. ( C ) KEGG analysis for differentially expressed genes found enrichment signaling pathways in tumor samples. ( D, E ) Heatmap displays the expression changes of cytokines after RRBP1 inhibition in MB49 cells and tumor tissues. ( F ) The Venn diagram illustrates the differentially expressed cytokines in both MB49 cells and tumor tissues after inhibition of RRBP1. ( G ) Representative images of IHC staining for RRBP1 and CXCL10 expression in BC samples. ( H ) The correlation between RRBP1 expression and CXCL10 expression was analyzed based on 96 patients from in-house BC cohort. Scale bar: 50 µm. ( I ) The mRNA expression of CXCL10 after genetic or pharmacological inhibition of RRBP1 in T24. ( J ) ELISA analysis of CXCL10 expression after genetic or pharmacological inhibition of RRBP1 in T24. ( K ) Distribution of RRBP1-binding peaks across CXCL10 by integrative genomics Viewer. ( L, M ) RIP analyses of MB49 cells or T24 cells were performed with an anti-RRBP1 antibody followed by qPCR analyses with primer against CXCL10 mRNA. ( N, O ) Knockdown of ENO1 to detect the CXCL10 mRNA expression levels in MB49 cells or T24 cells that were treated with actinomycin D for the indicated time. Data are represented as mean means±SD. Statistical analysis was performed using unpaired two-tailed t-test ( I, J, L, M, N, O ) or Spearman correlation analysis ( H ). The data presented represent one or three independent experiments. *p<0.05, ***p<0.001. BC, bladder cancer; mRNA, messenger RNA; qPCR, quantitative PCR; RRB1, ribosomal-binding protein 1; IHC, immunohistochemistry; KEGG, Kyoto Encyclopedia of Genes and Genomes.

Article Snippet: The concentrations of CXCL10 in the supernatant were measured using the Mouse CXCL10 ELISA Kit (R&D Systems, DY466-05) and Human CXCL10 ELISA Kit (Jianglai Biological, JL28903) according to the manufacturer’s instructions.

Techniques: Inhibition, Protein-Protein interactions, Expressing, Immunohistochemistry, Enzyme-linked Immunosorbent Assay, Binding Assay, Knockdown, Two Tailed Test, Real-time Polymerase Chain Reaction

RRBP1 inhibition promotes antitumor immunity via the CXCL10-CXCR3 axis in BC. ( A ) ScRNA-seq data showed the CXCR3 expression of CD8+T cells in shNC and shRRBP1 groups. ( B ) The correlation between CXCR3 expression and CXCL10 expression or activated CD8 + T cell based on 571 patients from TCGA-BLCA cohort and GSE13507 cohorts. ( C ) MB49 cells were co-cultured with CD8 + T cells, and tumor cells were stained with crystal violet. ( D ) Evaluation of the effect of genetic inhibition of RRBP1 on the cytotoxicity of CD8 + T cells in vitro conditioned culture model. ( E ) Schematic diagram of in vitro CD8 + T-cell migration assays. ( F ) The number of CD8 + T cells passing through the membrane of a Transwell system was analyzed by flow cytometry. ( G–I ) C57BL/6 mice were subcutaneously injected with 5×10 5 stable MB49 cells (shNC or shRRBP1 cells) (n=6). Tumor-bearing mice received intraperitoneal injection of either vehicle or anti-CXCL10 when the tumor volume reached a calculated average of 100 mm 3 . The tumor sizes ( G ), volumes ( H ), and weights ( I ) were measured. ( J ) Representative images of IHC and mIHC staining for CD8, CXCR3, CXCL10, IFN-γ, GZMB in different tumor tissues. ( K ) Flow cytometric analysis of tumor-infiltrating CD8 + T cells, CXCR3 + CD8 + T cells, IFN-γ + CD8 + T cells or GZMB + CD8 + T cells in distinct tumor tissues. Data are represented as mean means±SD. Statistical analysis was performed using unpaired two-tailed t-test ( D, F, I, K ) and two-way ANOVA with Tukey’s multiple comparison test ( H ). The data presented represent on one or three independent experiments. *p<0.01, **p<0.01, ***p<0.001. ANOVA, analysis of variance; BC, bladder cancer; GZMB, Granzyme B; IFN, interferon; RRBP1, ribosomal-binding protein 1; scRNA-seq, single-cell RNA sequencing; IHC, immunohistochemistry; mIHC, multiplex immunohistochemistry; BLCA, bladder urothelial carcinoma.

Journal: Journal for Immunotherapy of Cancer

Article Title: Targeting RRBP1 reverses immune evasion and enhances immunotherapy efficacy via the CXCL10-CXCR3 axis in bladder cancer

doi: 10.1136/jitc-2025-013809

Figure Lengend Snippet: RRBP1 inhibition promotes antitumor immunity via the CXCL10-CXCR3 axis in BC. ( A ) ScRNA-seq data showed the CXCR3 expression of CD8+T cells in shNC and shRRBP1 groups. ( B ) The correlation between CXCR3 expression and CXCL10 expression or activated CD8 + T cell based on 571 patients from TCGA-BLCA cohort and GSE13507 cohorts. ( C ) MB49 cells were co-cultured with CD8 + T cells, and tumor cells were stained with crystal violet. ( D ) Evaluation of the effect of genetic inhibition of RRBP1 on the cytotoxicity of CD8 + T cells in vitro conditioned culture model. ( E ) Schematic diagram of in vitro CD8 + T-cell migration assays. ( F ) The number of CD8 + T cells passing through the membrane of a Transwell system was analyzed by flow cytometry. ( G–I ) C57BL/6 mice were subcutaneously injected with 5×10 5 stable MB49 cells (shNC or shRRBP1 cells) (n=6). Tumor-bearing mice received intraperitoneal injection of either vehicle or anti-CXCL10 when the tumor volume reached a calculated average of 100 mm 3 . The tumor sizes ( G ), volumes ( H ), and weights ( I ) were measured. ( J ) Representative images of IHC and mIHC staining for CD8, CXCR3, CXCL10, IFN-γ, GZMB in different tumor tissues. ( K ) Flow cytometric analysis of tumor-infiltrating CD8 + T cells, CXCR3 + CD8 + T cells, IFN-γ + CD8 + T cells or GZMB + CD8 + T cells in distinct tumor tissues. Data are represented as mean means±SD. Statistical analysis was performed using unpaired two-tailed t-test ( D, F, I, K ) and two-way ANOVA with Tukey’s multiple comparison test ( H ). The data presented represent on one or three independent experiments. *p<0.01, **p<0.01, ***p<0.001. ANOVA, analysis of variance; BC, bladder cancer; GZMB, Granzyme B; IFN, interferon; RRBP1, ribosomal-binding protein 1; scRNA-seq, single-cell RNA sequencing; IHC, immunohistochemistry; mIHC, multiplex immunohistochemistry; BLCA, bladder urothelial carcinoma.

Techniques: Inhibition, Expressing, Cell Culture, Staining, In Vitro, Migration, Membrane, Flow Cytometry, Injection, Two Tailed Test, Comparison, Binding Assay, Single Cell, RNA Sequencing, Immunohistochemistry, Multiplex Assay

RRBP1 inhibition enhances response to anti-PD-L1 therapy in BC. ( A–D ) The protein expression of surface PD-L1 was analyzed in BC cells or tumor tissues by flow cytometry after RRBP1 inhibition and was shown as the mean fluorescence intensity. ( E–G ) C57BL/6 mice were subcutaneously injected with 5×10 5 stable MB49 cells (shNC or shRRBP1 cells) (n=6). Tumor-bearing mice were received intraperitoneal injection of either vehicle or anti-PD-L1 antibody when the tumor volume reached a calculated average of 100 mm 3 . The tumor sizes ( E ), volumes ( F ), and weights ( G ) were measured. ( H ) Representative images of IHC and mIHC staining for CD8, CXCR3, CXCL10, IFN-γ, GZMB in different tumor tissues. ( I ) Flow cytometric analysis of tumor-infiltrating CD8 + T cells, CXCR3 + CD8 + T cells, IFN-γ + CD8 + T cells or GZMB + CD8 + T cells in distinct tumor tissues. Data are represented as mean means±SD. Statistical analysis was performed using unpaired two-tailed t-test ( B, D, G, I ) and two-way ANOVA with Tukey’s multiple comparison test ( F ). The data presented represent on one or three independent experiments. *p<0.01, **p<0.01, ***p<0.001. ANOVA, analysis of variance; BC, bladder cancer; GZMB, Granzyme B; IFN, interferon; PD-L1, programmed death-ligand 1; RRBP1, ribosomal-binding protein 1; IHC, immunohistochemistry; mIHC, multiplex immunohistochemistry.

Journal: Journal for Immunotherapy of Cancer

Article Title: Targeting RRBP1 reverses immune evasion and enhances immunotherapy efficacy via the CXCL10-CXCR3 axis in bladder cancer

doi: 10.1136/jitc-2025-013809

Figure Lengend Snippet: RRBP1 inhibition enhances response to anti-PD-L1 therapy in BC. ( A–D ) The protein expression of surface PD-L1 was analyzed in BC cells or tumor tissues by flow cytometry after RRBP1 inhibition and was shown as the mean fluorescence intensity. ( E–G ) C57BL/6 mice were subcutaneously injected with 5×10 5 stable MB49 cells (shNC or shRRBP1 cells) (n=6). Tumor-bearing mice were received intraperitoneal injection of either vehicle or anti-PD-L1 antibody when the tumor volume reached a calculated average of 100 mm 3 . The tumor sizes ( E ), volumes ( F ), and weights ( G ) were measured. ( H ) Representative images of IHC and mIHC staining for CD8, CXCR3, CXCL10, IFN-γ, GZMB in different tumor tissues. ( I ) Flow cytometric analysis of tumor-infiltrating CD8 + T cells, CXCR3 + CD8 + T cells, IFN-γ + CD8 + T cells or GZMB + CD8 + T cells in distinct tumor tissues. Data are represented as mean means±SD. Statistical analysis was performed using unpaired two-tailed t-test ( B, D, G, I ) and two-way ANOVA with Tukey’s multiple comparison test ( F ). The data presented represent on one or three independent experiments. *p<0.01, **p<0.01, ***p<0.001. ANOVA, analysis of variance; BC, bladder cancer; GZMB, Granzyme B; IFN, interferon; PD-L1, programmed death-ligand 1; RRBP1, ribosomal-binding protein 1; IHC, immunohistochemistry; mIHC, multiplex immunohistochemistry.

Techniques: Inhibition, Expressing, Flow Cytometry, Fluorescence, Injection, Staining, Two Tailed Test, Comparison, Binding Assay, Immunohistochemistry, Multiplex Assay

Journal: Journal for Immunotherapy of Cancer

Article Title: Targeting RRBP1 reverses immune evasion and enhances immunotherapy efficacy via the CXCL10-CXCR3 axis in bladder cancer

doi: 10.1136/jitc-2025-013809

Journal: Journal for Immunotherapy of Cancer

Article Title: Targeting RRBP1 reverses immune evasion and enhances immunotherapy efficacy via the CXCL10-CXCR3 axis in bladder cancer

doi: 10.1136/jitc-2025-013809

Journal: Journal for Immunotherapy of Cancer

Article Title: Targeting RRBP1 reverses immune evasion and enhances immunotherapy efficacy via the CXCL10-CXCR3 axis in bladder cancer

doi: 10.1136/jitc-2025-013809

Techniques: Inhibition, Expressing, Flow Cytometry, Fluorescence, Injection, Staining, Two Tailed Test, Comparison, Binding Assay, Immunohistochemistry, Multiplex Assay

LNP-mRNA vaccine induces systemic innate immune activation. Mice were intramuscularly immunized by i.m. injection of LNP-RBD to the hind legs (2.5 µg to each leg). At the indicated time points (24, 48, 72 hours) post vaccination, the spleens were collected and analyzed by flow cytometry. (A) Representative flow-cytometry analysis dissecting the different DC populations in the spleens where population 1 represents DCs (CD11c high MHCII + ) and population 2 represents activated DCs (elevated MHC-II expression). (B) Quantification of activated DCs (population 2) in the spleens. (C) Ratio between the frequencies of cDC1 (CD8 + CD11b - ) and cDC2 (CD8 - CD11b + ) sub-populations among splenic DC (population 1). Activation of different cell populations was also quantified by CD86 expression on activated DCs (D) , monocytes (E) and PDCs (F) . Levels of IFNα (G) , CXCL10 (H) , IL-6 (I) and CCL2 (J) in the sera of vaccinated mice were measured at 6hr post immunization by ELISA. Gating strategy for A-F is presented in <xref ref-type=

Journal: Frontiers in Immunology

Article Title: The mRNA component of LNP-mRNA vaccines triggers IFNAR-dependent immune activation which attenuates the adaptive immune response

doi: 10.3389/fimmu.2025.1670350

Figure Lengend Snippet: LNP-mRNA vaccine induces systemic innate immune activation. Mice were intramuscularly immunized by i.m. injection of LNP-RBD to the hind legs (2.5 µg to each leg). At the indicated time points (24, 48, 72 hours) post vaccination, the spleens were collected and analyzed by flow cytometry. (A) Representative flow-cytometry analysis dissecting the different DC populations in the spleens where population 1 represents DCs (CD11c high MHCII + ) and population 2 represents activated DCs (elevated MHC-II expression). (B) Quantification of activated DCs (population 2) in the spleens. (C) Ratio between the frequencies of cDC1 (CD8 + CD11b - ) and cDC2 (CD8 - CD11b + ) sub-populations among splenic DC (population 1). Activation of different cell populations was also quantified by CD86 expression on activated DCs (D) , monocytes (E) and PDCs (F) . Levels of IFNα (G) , CXCL10 (H) , IL-6 (I) and CCL2 (J) in the sera of vaccinated mice were measured at 6hr post immunization by ELISA. Gating strategy for A-F is presented in Supplementary Figure S2 . Bars indicate means ± SEM from 4 animals per group. Each dot represents a single mouse. Statistical differences were determined using one-way ANOVA (B-F) or unpaired t tests (G–J) . P values: *P < 0.05, **P < 0.01, ***P < 0.001, and ns, not significant.

Article Snippet: Serum levels of IFNα, CXCL10, IL-6 and CCL2 were determines by ELISA kits (IFN-α-MFNAS0, CXCL10-DY466, IL-6-DY406, CCL2-DY479; R&D Systems, USA) according to the manufacturer’s instructions.

Techniques: Activation Assay, Injection, Flow Cytometry, Expressing, Enzyme-linked Immunosorbent Assay

Innate immune activation by LNP-mRNA is mRNA-dependent. Mice were vaccinated with empty LNPs (gray) or LNP-mRNA that encode to either RBD (red), Y. pestis F1 (green) or non-coding mRNA (blue). Control group was injected with PBS (black). dLNs and spleen were collected at 24hr post immunization for analyses of various cell populations by flow cytometry. Numbers of activated DCs in the dLNs (A) and Spleens (B) were quantified as described for <xref ref-type=

Figures 1 , 2 . Numbers of monocytes in the dLNs (C) and Spleens (D) were quantified as described for Figures 1 , 2 . Activation of different cell populations in the spleen was quantified by CD86 expression on activated DCs (E) , monocytes (F) , PDCs (G) and B-cells (H) . (I) Ratio between cDC1 and cDC2 subpopulations of non-activated DCs (population 1 in Figure 2 ). Levels of IFNα (J) , CXCL10 (K) , IL-6 (L) and CCL2 (M) in the sera of vaccinated mice were measured at 6hr post immunization by ELISA. Data are representative of two independent experiments. Bars indicate means ± SEM from 3–5 animals per group. Each dot represents a single mouse. Statistical differences were analyzed using one-way ANOVA. P values: *P < 0.05, **P < 0.01, ***P < 0.001, and ns, not significant. " width="100%" height="100%">

Journal: Frontiers in Immunology

Article Title: The mRNA component of LNP-mRNA vaccines triggers IFNAR-dependent immune activation which attenuates the adaptive immune response

doi: 10.3389/fimmu.2025.1670350

Figure Lengend Snippet: Innate immune activation by LNP-mRNA is mRNA-dependent. Mice were vaccinated with empty LNPs (gray) or LNP-mRNA that encode to either RBD (red), Y. pestis F1 (green) or non-coding mRNA (blue). Control group was injected with PBS (black). dLNs and spleen were collected at 24hr post immunization for analyses of various cell populations by flow cytometry. Numbers of activated DCs in the dLNs (A) and Spleens (B) were quantified as described for Figures 1 , 2 . Numbers of monocytes in the dLNs (C) and Spleens (D) were quantified as described for Figures 1 , 2 . Activation of different cell populations in the spleen was quantified by CD86 expression on activated DCs (E) , monocytes (F) , PDCs (G) and B-cells (H) . (I) Ratio between cDC1 and cDC2 subpopulations of non-activated DCs (population 1 in Figure 2 ). Levels of IFNα (J) , CXCL10 (K) , IL-6 (L) and CCL2 (M) in the sera of vaccinated mice were measured at 6hr post immunization by ELISA. Data are representative of two independent experiments. Bars indicate means ± SEM from 3–5 animals per group. Each dot represents a single mouse. Statistical differences were analyzed using one-way ANOVA. P values: *P < 0.05, **P < 0.01, ***P < 0.001, and ns, not significant.

Techniques: Activation Assay, Control, Injection, Flow Cytometry, Expressing, Enzyme-linked Immunosorbent Assay

Innate immune activation following LNP-mRNA vaccination is abrogated in IFNAR -/- mice. WT or IFNAR -/- mice were immunized with LNP-mRNA. A group of control WT mice was injected with PBS. dLNs and spleen were collected at 24hr post immunization for quantification of innate immune cell populations by flow cytometry as described in <xref ref-type=

Figure 1 , 2 . (A) Activated DCs in the dLN. (B) Activated DCs in the spleen. (C) Monocytes in the dLN. Activation of cell populations in the spleen was quantified by CD86 expression on activated DCs (D) , monocytes (E) , B-cells (F) and PDCs (G) . Levels of IFNα (H) , CXCL10 (I) , IL-6 (J) and CCL2 (K) in the sera of vaccinated mice were measured at 6hr post immunization by ELISA. Bars indicate means ± SEM from 5–7 animals per group. Each dot represents a single mouse. Statistical differences were analyzed using one-way ANOVA. P values: *P < 0.05, **P < 0.01, ***P < 0.001, and ns, not significant. " width="100%" height="100%">

Journal: Frontiers in Immunology

Article Title: The mRNA component of LNP-mRNA vaccines triggers IFNAR-dependent immune activation which attenuates the adaptive immune response

doi: 10.3389/fimmu.2025.1670350

Figure Lengend Snippet: Innate immune activation following LNP-mRNA vaccination is abrogated in IFNAR -/- mice. WT or IFNAR -/- mice were immunized with LNP-mRNA. A group of control WT mice was injected with PBS. dLNs and spleen were collected at 24hr post immunization for quantification of innate immune cell populations by flow cytometry as described in Figure 1 , 2 . (A) Activated DCs in the dLN. (B) Activated DCs in the spleen. (C) Monocytes in the dLN. Activation of cell populations in the spleen was quantified by CD86 expression on activated DCs (D) , monocytes (E) , B-cells (F) and PDCs (G) . Levels of IFNα (H) , CXCL10 (I) , IL-6 (J) and CCL2 (K) in the sera of vaccinated mice were measured at 6hr post immunization by ELISA. Bars indicate means ± SEM from 5–7 animals per group. Each dot represents a single mouse. Statistical differences were analyzed using one-way ANOVA. P values: *P < 0.05, **P < 0.01, ***P < 0.001, and ns, not significant.

Techniques: Activation Assay, Control, Injection, Flow Cytometry, Expressing, Enzyme-linked Immunosorbent Assay

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