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hek bluetm il 6  (InvivoGen)


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    InvivoGen hek bluetm il 6
    Innate activation was compared across mRNA–LNPs formulated with BP-104, SM-102, or ALC-0315 using NPmut mRNA as a common payload, and across matched empty LNP controls (iLNP; no mRNA) to isolate lipid-driven signaling. Reporter cells were exposed to a dose range of formulations (1 μg, 500 ng, 250 ng, 125 ng, and 62.5 ng; as indicated), and pathway activation was quantified as fold-change induction relative to baseline (dotted line). Bars denote mean responses with error bars indicating variability across replicates; selected pairwise comparisons are annotated with exact P values. a, NF-κB activation measured in THP1-Dual™ cells as induction of NF-κB–SEAP. Across doses, NPmut mRNA/LNPs and empty LNPs produced modest but consistent NF-κB induction, with broadly similar activation profiles across BP-104-, SM-102-, and ALC-0315–containing LNPs. <t>b,</t> <t>IL-6</t> pathway signaling measured in HEKBlue–IL-6 reporter cells as fold-change induction of IL-6–dependent signaling. All three ionizable lipid formulations elicited comparable IL-6 activation across the dilution series, and empty LNP controls also induced IL-6 signaling, indicating that both lipid composition and mRNA cargo contribute to pathway engagement. c, Type I interferon signaling measured in IFN-α/β reporter HEK293 cells as fold-change induction of IFN-I activity. NPmut mRNA/LNPs triggered IFN-I responses across lipids, with ALC-0315 producing slightly higher induction at select concentrations (P values shown). Empty LNPs also elicited measurable IFN-I signaling, consistent with lipid-dependent innate stimulation independent of mRNA. Collectively, these data show that BP-104 engages canonical innate immune pathways (NF-κB, IL-6, and type I interferon) at levels comparable to SM-102 and ALC-0315 under controlled dosing conditions, supporting its suitability as an ionizable lipid for mRNA–LNP vaccine delivery.
    Hek Bluetm Il 6, supplied by InvivoGen, used in various techniques. Bioz Stars score: 95/100, based on 62 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/hek+bluetm+il+6/HEK-Blue+IL-6+cells/bio_rxiv__64898__2026__01__17__699915-128-5-7
    Average 95 stars, based on 62 article reviews
    hek bluetm il 6 - by Bioz Stars, 2026-09
    95/100 stars

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    1) Product Images from "A modular mRNA–LNP vaccine platform enables integrated RNA, lipid and antigen design to protect against CCHFV"

    Article Title: A modular mRNA–LNP vaccine platform enables integrated RNA, lipid and antigen design to protect against CCHFV

    Journal: bioRxiv

    doi: 10.64898/2026.01.17.699915

    Innate activation was compared across mRNA–LNPs formulated with BP-104, SM-102, or ALC-0315 using NPmut mRNA as a common payload, and across matched empty LNP controls (iLNP; no mRNA) to isolate lipid-driven signaling. Reporter cells were exposed to a dose range of formulations (1 μg, 500 ng, 250 ng, 125 ng, and 62.5 ng; as indicated), and pathway activation was quantified as fold-change induction relative to baseline (dotted line). Bars denote mean responses with error bars indicating variability across replicates; selected pairwise comparisons are annotated with exact P values. a, NF-κB activation measured in THP1-Dual™ cells as induction of NF-κB–SEAP. Across doses, NPmut mRNA/LNPs and empty LNPs produced modest but consistent NF-κB induction, with broadly similar activation profiles across BP-104-, SM-102-, and ALC-0315–containing LNPs. b, IL-6 pathway signaling measured in HEKBlue–IL-6 reporter cells as fold-change induction of IL-6–dependent signaling. All three ionizable lipid formulations elicited comparable IL-6 activation across the dilution series, and empty LNP controls also induced IL-6 signaling, indicating that both lipid composition and mRNA cargo contribute to pathway engagement. c, Type I interferon signaling measured in IFN-α/β reporter HEK293 cells as fold-change induction of IFN-I activity. NPmut mRNA/LNPs triggered IFN-I responses across lipids, with ALC-0315 producing slightly higher induction at select concentrations (P values shown). Empty LNPs also elicited measurable IFN-I signaling, consistent with lipid-dependent innate stimulation independent of mRNA. Collectively, these data show that BP-104 engages canonical innate immune pathways (NF-κB, IL-6, and type I interferon) at levels comparable to SM-102 and ALC-0315 under controlled dosing conditions, supporting its suitability as an ionizable lipid for mRNA–LNP vaccine delivery.
    Figure Legend Snippet: Innate activation was compared across mRNA–LNPs formulated with BP-104, SM-102, or ALC-0315 using NPmut mRNA as a common payload, and across matched empty LNP controls (iLNP; no mRNA) to isolate lipid-driven signaling. Reporter cells were exposed to a dose range of formulations (1 μg, 500 ng, 250 ng, 125 ng, and 62.5 ng; as indicated), and pathway activation was quantified as fold-change induction relative to baseline (dotted line). Bars denote mean responses with error bars indicating variability across replicates; selected pairwise comparisons are annotated with exact P values. a, NF-κB activation measured in THP1-Dual™ cells as induction of NF-κB–SEAP. Across doses, NPmut mRNA/LNPs and empty LNPs produced modest but consistent NF-κB induction, with broadly similar activation profiles across BP-104-, SM-102-, and ALC-0315–containing LNPs. b, IL-6 pathway signaling measured in HEKBlue–IL-6 reporter cells as fold-change induction of IL-6–dependent signaling. All three ionizable lipid formulations elicited comparable IL-6 activation across the dilution series, and empty LNP controls also induced IL-6 signaling, indicating that both lipid composition and mRNA cargo contribute to pathway engagement. c, Type I interferon signaling measured in IFN-α/β reporter HEK293 cells as fold-change induction of IFN-I activity. NPmut mRNA/LNPs triggered IFN-I responses across lipids, with ALC-0315 producing slightly higher induction at select concentrations (P values shown). Empty LNPs also elicited measurable IFN-I signaling, consistent with lipid-dependent innate stimulation independent of mRNA. Collectively, these data show that BP-104 engages canonical innate immune pathways (NF-κB, IL-6, and type I interferon) at levels comparable to SM-102 and ALC-0315 under controlled dosing conditions, supporting its suitability as an ionizable lipid for mRNA–LNP vaccine delivery.

    Techniques Used: Activation Assay, Produced, Activity Assay

    Primary murine dendritic cells (DCs) were loaded with NPmut mRNA formulated in lipid nanoparticles (LNPs) containing BP-104, SM-102, or ALC-0315, then co-cultured with naïve CD4⁺ and CD8⁺ T cells to quantify intracellular cytokines and soluble mediators in supernatants. a, Frequencies of cytokine-positive CD4⁺ and CD8⁺ T cells measured by intracellular cytokine staining, including IFN-γ and TNF-α (top), IL-2⁺ CD8⁺ cells (bottom left), and IL-17A⁺ CD4⁺ cells (bottom right). Bars show group means with individual biological replicates overlaid; statistical comparisons and corresponding P values are indicated. Across formulations, NPmut mRNA/LNP-loaded DCs elicited Th1-skewed responses (IFN-γ and TNF-α) with a measurable IL-17A⁺ CD4⁺ population, whereas negative control cultures remained low. ALC-0315 drove the strongest IFN-γ⁺ and TNF-α⁺ T cell responses across CD4⁺ and CD8⁺ compartments and increased IL-17A⁺ CD4⁺ frequencies, BP-104 produced intermediate activation, and SM-102 was comparatively attenuated. Lipid-dependent differences were also evident for IL-2⁺ CD8⁺ responses, indicating differential programming of proliferative/expansion-associated outputs. b, Secreted cytokine and chemokine profiles in DC–T cell co-culture supernatants (mean fluorescence intensity, MFI) measured for inflammatory and recruitment-associated mediators, including TNF-α, CXCL1, IFN-γ, IL-12, CCL5, IL-4, CXCL10, GM-CSF, IL-10, IL-6, IP-10, and MCP-1. Error bars indicate variability across replicates; selected pairwise comparisons are annotated with P values. Supernatant signatures mirrored intracellular T cell phenotypes: ALC-0315 induced the most pronounced inflammatory/recruitment program, BP-104 generated a coherent but moderated profile, similar to SM-102. Together, these data show that ionizable lipid identity imprints innate cytokine/chemokine cues that scale and shape downstream Th1/Th17 polarization under fixed mRNA payload and DC-loading conditions.
    Figure Legend Snippet: Primary murine dendritic cells (DCs) were loaded with NPmut mRNA formulated in lipid nanoparticles (LNPs) containing BP-104, SM-102, or ALC-0315, then co-cultured with naïve CD4⁺ and CD8⁺ T cells to quantify intracellular cytokines and soluble mediators in supernatants. a, Frequencies of cytokine-positive CD4⁺ and CD8⁺ T cells measured by intracellular cytokine staining, including IFN-γ and TNF-α (top), IL-2⁺ CD8⁺ cells (bottom left), and IL-17A⁺ CD4⁺ cells (bottom right). Bars show group means with individual biological replicates overlaid; statistical comparisons and corresponding P values are indicated. Across formulations, NPmut mRNA/LNP-loaded DCs elicited Th1-skewed responses (IFN-γ and TNF-α) with a measurable IL-17A⁺ CD4⁺ population, whereas negative control cultures remained low. ALC-0315 drove the strongest IFN-γ⁺ and TNF-α⁺ T cell responses across CD4⁺ and CD8⁺ compartments and increased IL-17A⁺ CD4⁺ frequencies, BP-104 produced intermediate activation, and SM-102 was comparatively attenuated. Lipid-dependent differences were also evident for IL-2⁺ CD8⁺ responses, indicating differential programming of proliferative/expansion-associated outputs. b, Secreted cytokine and chemokine profiles in DC–T cell co-culture supernatants (mean fluorescence intensity, MFI) measured for inflammatory and recruitment-associated mediators, including TNF-α, CXCL1, IFN-γ, IL-12, CCL5, IL-4, CXCL10, GM-CSF, IL-10, IL-6, IP-10, and MCP-1. Error bars indicate variability across replicates; selected pairwise comparisons are annotated with P values. Supernatant signatures mirrored intracellular T cell phenotypes: ALC-0315 induced the most pronounced inflammatory/recruitment program, BP-104 generated a coherent but moderated profile, similar to SM-102. Together, these data show that ionizable lipid identity imprints innate cytokine/chemokine cues that scale and shape downstream Th1/Th17 polarization under fixed mRNA payload and DC-loading conditions.

    Techniques Used: Cell Culture, Staining, Negative Control, Produced, Activation Assay, Co-Culture Assay, Fluorescence, Generated

    Related Articles

    Activity Assay:

    Article Title: A modular mRNA–LNP vaccine platform enables integrated RNA, lipid and antigen design to protect against CCHFV
    Article Snippet: .. HEK-BlueTM IFN-α/β (InvivoGen, Cat# hkb-ifnabv2), HEK-BlueTM IL-6 (InvivoGen, Cat# hkb-hil6), and THP1-DualTM (InvivoGen, Cat# thpd-nfis) were employed to assess type I interferon activity and innate immune activation in response to NPmut mRNA–LNPs formulated with BP-104, SM-102, or ALC-0315. ..

    Activation Assay:

    Article Title: A modular mRNA–LNP vaccine platform enables integrated RNA, lipid and antigen design to protect against CCHFV
    Article Snippet: .. HEK-BlueTM IFN-α/β (InvivoGen, Cat# hkb-ifnabv2), HEK-BlueTM IL-6 (InvivoGen, Cat# hkb-hil6), and THP1-DualTM (InvivoGen, Cat# thpd-nfis) were employed to assess type I interferon activity and innate immune activation in response to NPmut mRNA–LNPs formulated with BP-104, SM-102, or ALC-0315. ..

    CCK-8 Assay:

    Article Title: Identification of histone deacetylase inhibitor targeting type I interferon and B-cell abnormalities in systemic lupus erythematosus.
    Article Snippet: THP1-Blue ISG cells purchased from InvivoGen (San Diego, CA, USA) and peripheral blood mononuclear cells (PBMCs) were seeded and treated with compounds from the Prestwick Chemical Library (Prestwick Chemical, San Diego, CA, USA) at 1 μM in the presence of resiquimod (R848; 10 μg/mL), 2’3’-cyclic GMP-AMP (2’3’-cGAMP; 5 μg/mL), or IFN-I (Universal IFN-I 200 U/mL) for 24 h. Universal IFN-I was used with the expectation of IFN-αA activity, confirmed in our previous experiments to exhibit stable effects. .. IFN-I production was evaluated using HEK-Blue IFN-α/β, HEK-BlueTM TNF-α, HEK-BlueTM IL-6, and B16-Blue IFN-α/β reporter cells (InvivoGen) as previously described1, and cell viability was measured using the cell counting kit-8 (Dojindo Laboratories, Tokyo, Japan). ..



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    Innate activation was compared across mRNA–LNPs formulated with BP-104, SM-102, or ALC-0315 using NPmut mRNA as a common payload, and across matched empty LNP controls (iLNP; no mRNA) to isolate lipid-driven signaling. Reporter cells were exposed to a dose range of formulations (1 μg, 500 ng, 250 ng, 125 ng, and 62.5 ng; as indicated), and pathway activation was quantified as fold-change induction relative to baseline (dotted line). Bars denote mean responses with error bars indicating variability across replicates; selected pairwise comparisons are annotated with exact P values. a, NF-κB activation measured in THP1-Dual™ cells as induction of NF-κB–SEAP. Across doses, NPmut mRNA/LNPs and empty LNPs produced modest but consistent NF-κB induction, with broadly similar activation profiles across BP-104-, SM-102-, and ALC-0315–containing LNPs. <t>b,</t> <t>IL-6</t> pathway signaling measured in HEKBlue–IL-6 reporter cells as fold-change induction of IL-6–dependent signaling. All three ionizable lipid formulations elicited comparable IL-6 activation across the dilution series, and empty LNP controls also induced IL-6 signaling, indicating that both lipid composition and mRNA cargo contribute to pathway engagement. c, Type I interferon signaling measured in IFN-α/β reporter HEK293 cells as fold-change induction of IFN-I activity. NPmut mRNA/LNPs triggered IFN-I responses across lipids, with ALC-0315 producing slightly higher induction at select concentrations (P values shown). Empty LNPs also elicited measurable IFN-I signaling, consistent with lipid-dependent innate stimulation independent of mRNA. Collectively, these data show that BP-104 engages canonical innate immune pathways (NF-κB, IL-6, and type I interferon) at levels comparable to SM-102 and ALC-0315 under controlled dosing conditions, supporting its suitability as an ionizable lipid for mRNA–LNP vaccine delivery.
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    Innate activation was compared across mRNA–LNPs formulated with BP-104, SM-102, or ALC-0315 using NPmut mRNA as a common payload, and across matched empty LNP controls (iLNP; no mRNA) to isolate lipid-driven signaling. Reporter cells were exposed to a dose range of formulations (1 μg, 500 ng, 250 ng, 125 ng, and 62.5 ng; as indicated), and pathway activation was quantified as fold-change induction relative to baseline (dotted line). Bars denote mean responses with error bars indicating variability across replicates; selected pairwise comparisons are annotated with exact P values. a, NF-κB activation measured in THP1-Dual™ cells as induction of NF-κB–SEAP. Across doses, NPmut mRNA/LNPs and empty LNPs produced modest but consistent NF-κB induction, with broadly similar activation profiles across BP-104-, SM-102-, and ALC-0315–containing LNPs. b, IL-6 pathway signaling measured in HEKBlue–IL-6 reporter cells as fold-change induction of IL-6–dependent signaling. All three ionizable lipid formulations elicited comparable IL-6 activation across the dilution series, and empty LNP controls also induced IL-6 signaling, indicating that both lipid composition and mRNA cargo contribute to pathway engagement. c, Type I interferon signaling measured in IFN-α/β reporter HEK293 cells as fold-change induction of IFN-I activity. NPmut mRNA/LNPs triggered IFN-I responses across lipids, with ALC-0315 producing slightly higher induction at select concentrations (P values shown). Empty LNPs also elicited measurable IFN-I signaling, consistent with lipid-dependent innate stimulation independent of mRNA. Collectively, these data show that BP-104 engages canonical innate immune pathways (NF-κB, IL-6, and type I interferon) at levels comparable to SM-102 and ALC-0315 under controlled dosing conditions, supporting its suitability as an ionizable lipid for mRNA–LNP vaccine delivery.

    Journal: bioRxiv

    Article Title: A modular mRNA–LNP vaccine platform enables integrated RNA, lipid and antigen design to protect against CCHFV

    doi: 10.64898/2026.01.17.699915

    Figure Lengend Snippet: Innate activation was compared across mRNA–LNPs formulated with BP-104, SM-102, or ALC-0315 using NPmut mRNA as a common payload, and across matched empty LNP controls (iLNP; no mRNA) to isolate lipid-driven signaling. Reporter cells were exposed to a dose range of formulations (1 μg, 500 ng, 250 ng, 125 ng, and 62.5 ng; as indicated), and pathway activation was quantified as fold-change induction relative to baseline (dotted line). Bars denote mean responses with error bars indicating variability across replicates; selected pairwise comparisons are annotated with exact P values. a, NF-κB activation measured in THP1-Dual™ cells as induction of NF-κB–SEAP. Across doses, NPmut mRNA/LNPs and empty LNPs produced modest but consistent NF-κB induction, with broadly similar activation profiles across BP-104-, SM-102-, and ALC-0315–containing LNPs. b, IL-6 pathway signaling measured in HEKBlue–IL-6 reporter cells as fold-change induction of IL-6–dependent signaling. All three ionizable lipid formulations elicited comparable IL-6 activation across the dilution series, and empty LNP controls also induced IL-6 signaling, indicating that both lipid composition and mRNA cargo contribute to pathway engagement. c, Type I interferon signaling measured in IFN-α/β reporter HEK293 cells as fold-change induction of IFN-I activity. NPmut mRNA/LNPs triggered IFN-I responses across lipids, with ALC-0315 producing slightly higher induction at select concentrations (P values shown). Empty LNPs also elicited measurable IFN-I signaling, consistent with lipid-dependent innate stimulation independent of mRNA. Collectively, these data show that BP-104 engages canonical innate immune pathways (NF-κB, IL-6, and type I interferon) at levels comparable to SM-102 and ALC-0315 under controlled dosing conditions, supporting its suitability as an ionizable lipid for mRNA–LNP vaccine delivery.

    Article Snippet: HEK-BlueTM IFN-α/β (InvivoGen, Cat# hkb-ifnabv2), HEK-BlueTM IL-6 (InvivoGen, Cat# hkb-hil6), and THP1-DualTM (InvivoGen, Cat# thpd-nfis) were employed to assess type I interferon activity and innate immune activation in response to NPmut mRNA–LNPs formulated with BP-104, SM-102, or ALC-0315.

    Techniques: Activation Assay, Produced, Activity Assay

    Primary murine dendritic cells (DCs) were loaded with NPmut mRNA formulated in lipid nanoparticles (LNPs) containing BP-104, SM-102, or ALC-0315, then co-cultured with naïve CD4⁺ and CD8⁺ T cells to quantify intracellular cytokines and soluble mediators in supernatants. a, Frequencies of cytokine-positive CD4⁺ and CD8⁺ T cells measured by intracellular cytokine staining, including IFN-γ and TNF-α (top), IL-2⁺ CD8⁺ cells (bottom left), and IL-17A⁺ CD4⁺ cells (bottom right). Bars show group means with individual biological replicates overlaid; statistical comparisons and corresponding P values are indicated. Across formulations, NPmut mRNA/LNP-loaded DCs elicited Th1-skewed responses (IFN-γ and TNF-α) with a measurable IL-17A⁺ CD4⁺ population, whereas negative control cultures remained low. ALC-0315 drove the strongest IFN-γ⁺ and TNF-α⁺ T cell responses across CD4⁺ and CD8⁺ compartments and increased IL-17A⁺ CD4⁺ frequencies, BP-104 produced intermediate activation, and SM-102 was comparatively attenuated. Lipid-dependent differences were also evident for IL-2⁺ CD8⁺ responses, indicating differential programming of proliferative/expansion-associated outputs. b, Secreted cytokine and chemokine profiles in DC–T cell co-culture supernatants (mean fluorescence intensity, MFI) measured for inflammatory and recruitment-associated mediators, including TNF-α, CXCL1, IFN-γ, IL-12, CCL5, IL-4, CXCL10, GM-CSF, IL-10, IL-6, IP-10, and MCP-1. Error bars indicate variability across replicates; selected pairwise comparisons are annotated with P values. Supernatant signatures mirrored intracellular T cell phenotypes: ALC-0315 induced the most pronounced inflammatory/recruitment program, BP-104 generated a coherent but moderated profile, similar to SM-102. Together, these data show that ionizable lipid identity imprints innate cytokine/chemokine cues that scale and shape downstream Th1/Th17 polarization under fixed mRNA payload and DC-loading conditions.

    Journal: bioRxiv

    Article Title: A modular mRNA–LNP vaccine platform enables integrated RNA, lipid and antigen design to protect against CCHFV

    doi: 10.64898/2026.01.17.699915

    Figure Lengend Snippet: Primary murine dendritic cells (DCs) were loaded with NPmut mRNA formulated in lipid nanoparticles (LNPs) containing BP-104, SM-102, or ALC-0315, then co-cultured with naïve CD4⁺ and CD8⁺ T cells to quantify intracellular cytokines and soluble mediators in supernatants. a, Frequencies of cytokine-positive CD4⁺ and CD8⁺ T cells measured by intracellular cytokine staining, including IFN-γ and TNF-α (top), IL-2⁺ CD8⁺ cells (bottom left), and IL-17A⁺ CD4⁺ cells (bottom right). Bars show group means with individual biological replicates overlaid; statistical comparisons and corresponding P values are indicated. Across formulations, NPmut mRNA/LNP-loaded DCs elicited Th1-skewed responses (IFN-γ and TNF-α) with a measurable IL-17A⁺ CD4⁺ population, whereas negative control cultures remained low. ALC-0315 drove the strongest IFN-γ⁺ and TNF-α⁺ T cell responses across CD4⁺ and CD8⁺ compartments and increased IL-17A⁺ CD4⁺ frequencies, BP-104 produced intermediate activation, and SM-102 was comparatively attenuated. Lipid-dependent differences were also evident for IL-2⁺ CD8⁺ responses, indicating differential programming of proliferative/expansion-associated outputs. b, Secreted cytokine and chemokine profiles in DC–T cell co-culture supernatants (mean fluorescence intensity, MFI) measured for inflammatory and recruitment-associated mediators, including TNF-α, CXCL1, IFN-γ, IL-12, CCL5, IL-4, CXCL10, GM-CSF, IL-10, IL-6, IP-10, and MCP-1. Error bars indicate variability across replicates; selected pairwise comparisons are annotated with P values. Supernatant signatures mirrored intracellular T cell phenotypes: ALC-0315 induced the most pronounced inflammatory/recruitment program, BP-104 generated a coherent but moderated profile, similar to SM-102. Together, these data show that ionizable lipid identity imprints innate cytokine/chemokine cues that scale and shape downstream Th1/Th17 polarization under fixed mRNA payload and DC-loading conditions.

    Article Snippet: HEK-BlueTM IFN-α/β (InvivoGen, Cat# hkb-ifnabv2), HEK-BlueTM IL-6 (InvivoGen, Cat# hkb-hil6), and THP1-DualTM (InvivoGen, Cat# thpd-nfis) were employed to assess type I interferon activity and innate immune activation in response to NPmut mRNA–LNPs formulated with BP-104, SM-102, or ALC-0315.

    Techniques: Cell Culture, Staining, Negative Control, Produced, Activation Assay, Co-Culture Assay, Fluorescence, Generated