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anti il17a  (Bio X Cell)


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    Structured Review

    Bio X Cell anti il17a
    To model EA or MGA respectively, Balb/c or Il4ra -/- mice were given five intranasal (i.n.) challenges with 100ug house dust mite (HDM) extract every week (followed by two days resting) for three consecutive weeks. A final i.n. HDM challenge was given 24 hours prior to harvest. ( A ) Lung sections were stained and representative Masson trichrome (collagen), α-smooth muscle actin (αSMA), and hematoxylin and eosin (H&E) sections and accompanying quantifications are shown. ( B ) Airway resistance to increasing doses of methacholine exposure (6-8 mice per group). (C) Expression of mRNA for IL13 and IL17, assessed by quantitative PCR analyses of lung samples. mRNA expression was calculated relative to GAPDH for 5 mice per group. ( D ) Number of neutrophils or eosinophils in the left lung lobe of EA or MGA induced mice, as assessed by flow cytometry. ( E ) MGA-induced animals were treated with 50ug dexamethasone intratracheally one hour prior to each allergen challenge, beginning on day 7. Lung sections were stained and representative Masson trichrome and αSMA sections and accompanying quantifications are shown. ( F ) Number of neutrophils or eosinophils in the left lung lobe of MGA induced mice treated with or without dexamethasone, as assessed by flow cytometry. ( G ) MGA-induced animals were treated with <t>100ug</t> <t>anti-IL17A</t> or matching isotype control i.p. beginning on day 7 and continuing every other day until harvest. Lung sections were stained, and representative H&E sections and accompanying quantifications are shown. Trichrome data show area of interest values covering full lung section of 6 individual mice per condition. αSMA data show mean values of all bronchi scored from 6 mice per condition. Data are representative of 3 independent experiments. *P < 0.05, **P < 0.005, ***P < 0.0005, ****P < 0.00005; HPF, high-power field; ns, nonsignificant.
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    Images

    1) Product Images from "The metabolic reprogramming of T cells controls airway remodeling in severe asthma"

    Article Title: The metabolic reprogramming of T cells controls airway remodeling in severe asthma

    Journal: bioRxiv

    doi: 10.64898/2026.03.19.712985

    To model EA or MGA respectively, Balb/c or Il4ra -/- mice were given five intranasal (i.n.) challenges with 100ug house dust mite (HDM) extract every week (followed by two days resting) for three consecutive weeks. A final i.n. HDM challenge was given 24 hours prior to harvest. ( A ) Lung sections were stained and representative Masson trichrome (collagen), α-smooth muscle actin (αSMA), and hematoxylin and eosin (H&E) sections and accompanying quantifications are shown. ( B ) Airway resistance to increasing doses of methacholine exposure (6-8 mice per group). (C) Expression of mRNA for IL13 and IL17, assessed by quantitative PCR analyses of lung samples. mRNA expression was calculated relative to GAPDH for 5 mice per group. ( D ) Number of neutrophils or eosinophils in the left lung lobe of EA or MGA induced mice, as assessed by flow cytometry. ( E ) MGA-induced animals were treated with 50ug dexamethasone intratracheally one hour prior to each allergen challenge, beginning on day 7. Lung sections were stained and representative Masson trichrome and αSMA sections and accompanying quantifications are shown. ( F ) Number of neutrophils or eosinophils in the left lung lobe of MGA induced mice treated with or without dexamethasone, as assessed by flow cytometry. ( G ) MGA-induced animals were treated with 100ug anti-IL17A or matching isotype control i.p. beginning on day 7 and continuing every other day until harvest. Lung sections were stained, and representative H&E sections and accompanying quantifications are shown. Trichrome data show area of interest values covering full lung section of 6 individual mice per condition. αSMA data show mean values of all bronchi scored from 6 mice per condition. Data are representative of 3 independent experiments. *P < 0.05, **P < 0.005, ***P < 0.0005, ****P < 0.00005; HPF, high-power field; ns, nonsignificant.
    Figure Legend Snippet: To model EA or MGA respectively, Balb/c or Il4ra -/- mice were given five intranasal (i.n.) challenges with 100ug house dust mite (HDM) extract every week (followed by two days resting) for three consecutive weeks. A final i.n. HDM challenge was given 24 hours prior to harvest. ( A ) Lung sections were stained and representative Masson trichrome (collagen), α-smooth muscle actin (αSMA), and hematoxylin and eosin (H&E) sections and accompanying quantifications are shown. ( B ) Airway resistance to increasing doses of methacholine exposure (6-8 mice per group). (C) Expression of mRNA for IL13 and IL17, assessed by quantitative PCR analyses of lung samples. mRNA expression was calculated relative to GAPDH for 5 mice per group. ( D ) Number of neutrophils or eosinophils in the left lung lobe of EA or MGA induced mice, as assessed by flow cytometry. ( E ) MGA-induced animals were treated with 50ug dexamethasone intratracheally one hour prior to each allergen challenge, beginning on day 7. Lung sections were stained and representative Masson trichrome and αSMA sections and accompanying quantifications are shown. ( F ) Number of neutrophils or eosinophils in the left lung lobe of MGA induced mice treated with or without dexamethasone, as assessed by flow cytometry. ( G ) MGA-induced animals were treated with 100ug anti-IL17A or matching isotype control i.p. beginning on day 7 and continuing every other day until harvest. Lung sections were stained, and representative H&E sections and accompanying quantifications are shown. Trichrome data show area of interest values covering full lung section of 6 individual mice per condition. αSMA data show mean values of all bronchi scored from 6 mice per condition. Data are representative of 3 independent experiments. *P < 0.05, **P < 0.005, ***P < 0.0005, ****P < 0.00005; HPF, high-power field; ns, nonsignificant.

    Techniques Used: Staining, Expressing, Real-time Polymerase Chain Reaction, Flow Cytometry, Control



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    Sartorius AG anti il 6 anti il17a bispecific antibody cpbt0853
    Expression and purification of <t>CPBT0853.</t> Panel ( A ) is a schematic representation of the generation of the bispecific antibody. Following phage display selection, and VHHs’ identification, the first produced version of bispecific antibody, named CPBT0853, was in the IgG1 format. The antibody was then reformatted into an IgG4 version (CPBT1174), and humanization was subsequently performed by substituting specific amino acids to reduce immunogenicity (CPBT1269). Panel ( B ) shows the SDS-PAGE analysis under non-reducing conditions, illustrating the expression profile of CPBT0853 over seven days following transient transfection in ExpiCHO-S cells. An arrow indicates the expected protein band. Panel ( C ) presents a representative chromatogram from the affinity purification step using MabCaptureC resin. Panel ( D ) displays the size-exclusion chromatography (SEC) profile of the final purified CPBT0853, confirming the high homogeneity of the sample.
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    Expression and purification of <t>CPBT0853.</t> Panel ( A ) is a schematic representation of the generation of the bispecific antibody. Following phage display selection, and VHHs’ identification, the first produced version of bispecific antibody, named CPBT0853, was in the IgG1 format. The antibody was then reformatted into an IgG4 version (CPBT1174), and humanization was subsequently performed by substituting specific amino acids to reduce immunogenicity (CPBT1269). Panel ( B ) shows the SDS-PAGE analysis under non-reducing conditions, illustrating the expression profile of CPBT0853 over seven days following transient transfection in ExpiCHO-S cells. An arrow indicates the expected protein band. Panel ( C ) presents a representative chromatogram from the affinity purification step using MabCaptureC resin. Panel ( D ) displays the size-exclusion chromatography (SEC) profile of the final purified CPBT0853, confirming the high homogeneity of the sample.
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    Bio X Cell anti il17a
    To model EA or MGA respectively, Balb/c or Il4ra -/- mice were given five intranasal (i.n.) challenges with 100ug house dust mite (HDM) extract every week (followed by two days resting) for three consecutive weeks. A final i.n. HDM challenge was given 24 hours prior to harvest. ( A ) Lung sections were stained and representative Masson trichrome (collagen), α-smooth muscle actin (αSMA), and hematoxylin and eosin (H&E) sections and accompanying quantifications are shown. ( B ) Airway resistance to increasing doses of methacholine exposure (6-8 mice per group). (C) Expression of mRNA for IL13 and IL17, assessed by quantitative PCR analyses of lung samples. mRNA expression was calculated relative to GAPDH for 5 mice per group. ( D ) Number of neutrophils or eosinophils in the left lung lobe of EA or MGA induced mice, as assessed by flow cytometry. ( E ) MGA-induced animals were treated with 50ug dexamethasone intratracheally one hour prior to each allergen challenge, beginning on day 7. Lung sections were stained and representative Masson trichrome and αSMA sections and accompanying quantifications are shown. ( F ) Number of neutrophils or eosinophils in the left lung lobe of MGA induced mice treated with or without dexamethasone, as assessed by flow cytometry. ( G ) MGA-induced animals were treated with <t>100ug</t> <t>anti-IL17A</t> or matching isotype control i.p. beginning on day 7 and continuing every other day until harvest. Lung sections were stained, and representative H&E sections and accompanying quantifications are shown. Trichrome data show area of interest values covering full lung section of 6 individual mice per condition. αSMA data show mean values of all bronchi scored from 6 mice per condition. Data are representative of 3 independent experiments. *P < 0.05, **P < 0.005, ***P < 0.0005, ****P < 0.00005; HPF, high-power field; ns, nonsignificant.
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    To model EA or MGA respectively, Balb/c or Il4ra -/- mice were given five intranasal (i.n.) challenges with 100ug house dust mite (HDM) extract every week (followed by two days resting) for three consecutive weeks. A final i.n. HDM challenge was given 24 hours prior to harvest. ( A ) Lung sections were stained and representative Masson trichrome (collagen), α-smooth muscle actin (αSMA), and hematoxylin and eosin (H&E) sections and accompanying quantifications are shown. ( B ) Airway resistance to increasing doses of methacholine exposure (6-8 mice per group). (C) Expression of mRNA for IL13 and IL17, assessed by quantitative PCR analyses of lung samples. mRNA expression was calculated relative to GAPDH for 5 mice per group. ( D ) Number of neutrophils or eosinophils in the left lung lobe of EA or MGA induced mice, as assessed by flow cytometry. ( E ) MGA-induced animals were treated with 50ug dexamethasone intratracheally one hour prior to each allergen challenge, beginning on day 7. Lung sections were stained and representative Masson trichrome and αSMA sections and accompanying quantifications are shown. ( F ) Number of neutrophils or eosinophils in the left lung lobe of MGA induced mice treated with or without dexamethasone, as assessed by flow cytometry. ( G ) MGA-induced animals were treated with <t>100ug</t> <t>anti-IL17A</t> or matching isotype control i.p. beginning on day 7 and continuing every other day until harvest. Lung sections were stained, and representative H&E sections and accompanying quantifications are shown. Trichrome data show area of interest values covering full lung section of 6 individual mice per condition. αSMA data show mean values of all bronchi scored from 6 mice per condition. Data are representative of 3 independent experiments. *P < 0.05, **P < 0.005, ***P < 0.0005, ****P < 0.00005; HPF, high-power field; ns, nonsignificant.
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    Proteintech il17a
    To model EA or MGA respectively, Balb/c or Il4ra -/- mice were given five intranasal (i.n.) challenges with 100ug house dust mite (HDM) extract every week (followed by two days resting) for three consecutive weeks. A final i.n. HDM challenge was given 24 hours prior to harvest. ( A ) Lung sections were stained and representative Masson trichrome (collagen), α-smooth muscle actin (αSMA), and hematoxylin and eosin (H&E) sections and accompanying quantifications are shown. ( B ) Airway resistance to increasing doses of methacholine exposure (6-8 mice per group). (C) Expression of mRNA for IL13 and IL17, assessed by quantitative PCR analyses of lung samples. mRNA expression was calculated relative to GAPDH for 5 mice per group. ( D ) Number of neutrophils or eosinophils in the left lung lobe of EA or MGA induced mice, as assessed by flow cytometry. ( E ) MGA-induced animals were treated with 50ug dexamethasone intratracheally one hour prior to each allergen challenge, beginning on day 7. Lung sections were stained and representative Masson trichrome and αSMA sections and accompanying quantifications are shown. ( F ) Number of neutrophils or eosinophils in the left lung lobe of MGA induced mice treated with or without dexamethasone, as assessed by flow cytometry. ( G ) MGA-induced animals were treated with <t>100ug</t> <t>anti-IL17A</t> or matching isotype control i.p. beginning on day 7 and continuing every other day until harvest. Lung sections were stained, and representative H&E sections and accompanying quantifications are shown. Trichrome data show area of interest values covering full lung section of 6 individual mice per condition. αSMA data show mean values of all bronchi scored from 6 mice per condition. Data are representative of 3 independent experiments. *P < 0.05, **P < 0.005, ***P < 0.0005, ****P < 0.00005; HPF, high-power field; ns, nonsignificant.
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    Antagonizing IL-17A significantly reduces oxidative stress production in whole blood of C57BL/6J mice treated with Ang II over one week, attenuates vascular inflammation based on a trend, and has no impact on vascular dysfunction development. ( A ) Acetylcholine induced vascular relaxation in C57BL/6J mice, in C57BL/6J + Ang II mice, and in C57BL/6J + Ang II mice treated with either 60 µg/g bodyweight of <t>an</t> <t>anti-IL17A</t> or isotype control antibody over one week, n = 3–8 mice per group based on two independent experiments, two-way ANOVA with Bonferroni multiple comparison test. Black stars show the significancy between C57BL/6J and C57BL/6J + Ang II + ISO treated mice. Blue stars demonstrate the significancy between C57BL/6J versus C57BL/6J + Ang II + anti-IL17A treated mice. Black ### show the significancy between C57BL/6J and C57BL/6J + Ang II treated mice. (**/## p ≤ 0.01; ***/### p < 0.001). ( B ) ROS/RNS measurement in whole blood after 10 min of PDBu stimulation. Partially repeated measurements of pooled samples, n = 6–7 mice per group based on two independent experiments, one-way ANOVA with Bonferroni’s posttest. ( C ) Aortic inflammation detected via flow cytometry (gating strategy as described in ), n = 6–8 mice per group based on independent experiments, Kruskal–Wallis one-way ANOVA with Dunn’s posttest. All data are shown as the mean ± SEM. * p ≤ 0.05, ** p ≤ 0.01.
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    Bio X Cell il17a
    Memory versus naïve T cell responses following CLP. Twenty-four hrs. following sham procedure or CLP in C57Bl/6 mice, T cell cytokine production in response to in vitro T cell receptor stimulation were assessed. A Percentage of memory (CD44 + /CD11 + ) and naïve (CD44 − /CD11a − ) splenic (Left) or hepatic (Right) CD4 (Top) and CD8 (Bottom) T cells producing IFNγ, IL2, <t>IL17A</t> or TNF. Gating: FSC/SSC, Singlets, Live, CD90/CD4 or CD90/CD8, CD44/CD11a, IFNγ, IL2, IL17A or TNF. IL17A numbers displayed graphically following multiplication by 10 for clarity. Comparisons made by two-way ANOVA comparing CLP/Sham and Memory/Naïve. * = p < 0.05 for interaction effect, # = p < 0.05 for CLP effect, ^ = p < 0.05 for Memory effect. Analyzed by 2-way ANOVA. Figures representative of 2 independent experiments. N = 3/group. B Pie graphs demonstrating the percentage of splenic memory (CD44 + /CD11 + ) and naïve (CD44 − /CD11a − ) CD4 and CD8 T cells producing one cytokine (Red), two cytokines (Blue), or three cytokines (Yellow) in response to in vitro T cell receptor stimulation. CD4 and CD8 T cell responses analyzed separately by 3-way ANOVA. N = 3/group. Gating: FSC/SSC, Singlets, Live Cells, CD90/CD4 or CD90/CD8, IFNγ, IL2, or TNF
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    Memory versus naïve T cell responses following CLP. Twenty-four hrs. following sham procedure or CLP in C57Bl/6 mice, T cell cytokine production in response to in vitro T cell receptor stimulation were assessed. A Percentage of memory (CD44 + /CD11 + ) and naïve (CD44 − /CD11a − ) splenic (Left) or hepatic (Right) CD4 (Top) and CD8 (Bottom) T cells producing IFNγ, IL2, <t>IL17A</t> or TNF. Gating: FSC/SSC, Singlets, Live, CD90/CD4 or CD90/CD8, CD44/CD11a, IFNγ, IL2, IL17A or TNF. IL17A numbers displayed graphically following multiplication by 10 for clarity. Comparisons made by two-way ANOVA comparing CLP/Sham and Memory/Naïve. * = p < 0.05 for interaction effect, # = p < 0.05 for CLP effect, ^ = p < 0.05 for Memory effect. Analyzed by 2-way ANOVA. Figures representative of 2 independent experiments. N = 3/group. B Pie graphs demonstrating the percentage of splenic memory (CD44 + /CD11 + ) and naïve (CD44 − /CD11a − ) CD4 and CD8 T cells producing one cytokine (Red), two cytokines (Blue), or three cytokines (Yellow) in response to in vitro T cell receptor stimulation. CD4 and CD8 T cell responses analyzed separately by 3-way ANOVA. N = 3/group. Gating: FSC/SSC, Singlets, Live Cells, CD90/CD4 or CD90/CD8, IFNγ, IL2, or TNF
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    Image Search Results


    Expression and purification of CPBT0853. Panel ( A ) is a schematic representation of the generation of the bispecific antibody. Following phage display selection, and VHHs’ identification, the first produced version of bispecific antibody, named CPBT0853, was in the IgG1 format. The antibody was then reformatted into an IgG4 version (CPBT1174), and humanization was subsequently performed by substituting specific amino acids to reduce immunogenicity (CPBT1269). Panel ( B ) shows the SDS-PAGE analysis under non-reducing conditions, illustrating the expression profile of CPBT0853 over seven days following transient transfection in ExpiCHO-S cells. An arrow indicates the expected protein band. Panel ( C ) presents a representative chromatogram from the affinity purification step using MabCaptureC resin. Panel ( D ) displays the size-exclusion chromatography (SEC) profile of the final purified CPBT0853, confirming the high homogeneity of the sample.

    Journal: Antibodies

    Article Title: Development of Bispecific Antibody Targeting Human IL-17A and IL-6

    doi: 10.3390/antib15020029

    Figure Lengend Snippet: Expression and purification of CPBT0853. Panel ( A ) is a schematic representation of the generation of the bispecific antibody. Following phage display selection, and VHHs’ identification, the first produced version of bispecific antibody, named CPBT0853, was in the IgG1 format. The antibody was then reformatted into an IgG4 version (CPBT1174), and humanization was subsequently performed by substituting specific amino acids to reduce immunogenicity (CPBT1269). Panel ( B ) shows the SDS-PAGE analysis under non-reducing conditions, illustrating the expression profile of CPBT0853 over seven days following transient transfection in ExpiCHO-S cells. An arrow indicates the expected protein band. Panel ( C ) presents a representative chromatogram from the affinity purification step using MabCaptureC resin. Panel ( D ) displays the size-exclusion chromatography (SEC) profile of the final purified CPBT0853, confirming the high homogeneity of the sample.

    Article Snippet: The binding of human, cynomolgus monkey ( Macaca fascicularis ), and mouse IL-6 and IL-17A (ACROBiosystems), human complex IL-17A/F (R&D System, Minneapolis, MN, USA) and human IL-17E and IL-17F (ACROBiosystems) to the anti-IL-6/anti-IL17A bispecific antibody CPBT0853 was analyzed using an Octet RED96 instrument (Sartorius AG).

    Techniques: Expressing, Purification, Selection, Produced, Immunopeptidomics, SDS Page, Transfection, Affinity Purification, Size-exclusion Chromatography

    Purity analysis of CPBT0853. ( A ) Representative chromatogram obtained from capillary electrophoresis, showing the purity profile of the CPBT853 sample. ( B ) The corresponding electropherogram, providing a visual representation of the separations of the final product differentially treated, as indicated. Each subsequent line in the electropherogram ( B ) corresponds to the following peak marked in the red box ( A ).

    Journal: Antibodies

    Article Title: Development of Bispecific Antibody Targeting Human IL-17A and IL-6

    doi: 10.3390/antib15020029

    Figure Lengend Snippet: Purity analysis of CPBT0853. ( A ) Representative chromatogram obtained from capillary electrophoresis, showing the purity profile of the CPBT853 sample. ( B ) The corresponding electropherogram, providing a visual representation of the separations of the final product differentially treated, as indicated. Each subsequent line in the electropherogram ( B ) corresponds to the following peak marked in the red box ( A ).

    Article Snippet: The binding of human, cynomolgus monkey ( Macaca fascicularis ), and mouse IL-6 and IL-17A (ACROBiosystems), human complex IL-17A/F (R&D System, Minneapolis, MN, USA) and human IL-17E and IL-17F (ACROBiosystems) to the anti-IL-6/anti-IL17A bispecific antibody CPBT0853 was analyzed using an Octet RED96 instrument (Sartorius AG).

    Techniques: Electrophoresis

    Biophysical characterization of CPBT0853 using the Uncle platform. ( A ) Thermal stability and aggregation analysis of CPBT853 assessed using fluorescence and static light scattering (SLS) to determine melting temperature (T m ) and aggregation onset temperature (T agg ), respectively. ( B ) Dynamic light scattering (DLS) measurements performed at 25 °C and 95 °C, demonstrating the hydrodynamic radius and polydispersity index (PDI) of the sample under native and heat-stressed conditions in three technical repetitions.

    Journal: Antibodies

    Article Title: Development of Bispecific Antibody Targeting Human IL-17A and IL-6

    doi: 10.3390/antib15020029

    Figure Lengend Snippet: Biophysical characterization of CPBT0853 using the Uncle platform. ( A ) Thermal stability and aggregation analysis of CPBT853 assessed using fluorescence and static light scattering (SLS) to determine melting temperature (T m ) and aggregation onset temperature (T agg ), respectively. ( B ) Dynamic light scattering (DLS) measurements performed at 25 °C and 95 °C, demonstrating the hydrodynamic radius and polydispersity index (PDI) of the sample under native and heat-stressed conditions in three technical repetitions.

    Article Snippet: The binding of human, cynomolgus monkey ( Macaca fascicularis ), and mouse IL-6 and IL-17A (ACROBiosystems), human complex IL-17A/F (R&D System, Minneapolis, MN, USA) and human IL-17E and IL-17F (ACROBiosystems) to the anti-IL-6/anti-IL17A bispecific antibody CPBT0853 was analyzed using an Octet RED96 instrument (Sartorius AG).

    Techniques: Fluorescence

    Binding affinity analysis of the CPBT0853 bispecific antibody. Representative bio-layer interferometry (BLI) binding curves for CPBT0853 interacting with human IL-17A ( A ), human IL-6 ( B ), human IL-17A/F heterodimer ( C ), cynomolgus monkey IL-17A ( D ), and cynomolgus monkey IL-6 ( E ) are shown. The absence of binding is demonstrated by the lack of interaction between CPBT0853 and mouse IL-6 ( F ).

    Journal: Antibodies

    Article Title: Development of Bispecific Antibody Targeting Human IL-17A and IL-6

    doi: 10.3390/antib15020029

    Figure Lengend Snippet: Binding affinity analysis of the CPBT0853 bispecific antibody. Representative bio-layer interferometry (BLI) binding curves for CPBT0853 interacting with human IL-17A ( A ), human IL-6 ( B ), human IL-17A/F heterodimer ( C ), cynomolgus monkey IL-17A ( D ), and cynomolgus monkey IL-6 ( E ) are shown. The absence of binding is demonstrated by the lack of interaction between CPBT0853 and mouse IL-6 ( F ).

    Article Snippet: The binding of human, cynomolgus monkey ( Macaca fascicularis ), and mouse IL-6 and IL-17A (ACROBiosystems), human complex IL-17A/F (R&D System, Minneapolis, MN, USA) and human IL-17E and IL-17F (ACROBiosystems) to the anti-IL-6/anti-IL17A bispecific antibody CPBT0853 was analyzed using an Octet RED96 instrument (Sartorius AG).

    Techniques: Binding Assay

    Blocking activity of the bispecific antibody CPBT0853 measured by bio-layer interferometry (BLI). Bar graphs represent quantitative data derived from BLI sensorgrams showing the effect of increasing concentrations of CPBT0853 on the binding of IL-17A ( A ) or IL-6 ( B ) to their respective receptors. The measured response [nm], reflecting the amount of receptor bound to the immobilized cytokine, decreases with increasing antibody concentration, indicating dose-dependent inhibition of cytokine–receptor interactions. Data represent mean ± SD from three independent experiments.

    Journal: Antibodies

    Article Title: Development of Bispecific Antibody Targeting Human IL-17A and IL-6

    doi: 10.3390/antib15020029

    Figure Lengend Snippet: Blocking activity of the bispecific antibody CPBT0853 measured by bio-layer interferometry (BLI). Bar graphs represent quantitative data derived from BLI sensorgrams showing the effect of increasing concentrations of CPBT0853 on the binding of IL-17A ( A ) or IL-6 ( B ) to their respective receptors. The measured response [nm], reflecting the amount of receptor bound to the immobilized cytokine, decreases with increasing antibody concentration, indicating dose-dependent inhibition of cytokine–receptor interactions. Data represent mean ± SD from three independent experiments.

    Article Snippet: The binding of human, cynomolgus monkey ( Macaca fascicularis ), and mouse IL-6 and IL-17A (ACROBiosystems), human complex IL-17A/F (R&D System, Minneapolis, MN, USA) and human IL-17E and IL-17F (ACROBiosystems) to the anti-IL-6/anti-IL17A bispecific antibody CPBT0853 was analyzed using an Octet RED96 instrument (Sartorius AG).

    Techniques: Blocking Assay, Activity Assay, Derivative Assay, Binding Assay, Concentration Assay, Inhibition

    Neutralization potency of CPBT0853 targeting IL-17A ( A ) and IL-6, IL-17A. Representative graphs show IC 50 analysis performed using a reporter cell assay. For comparison, parental VHHs and monospecific referential antibodies were used. The cellular response, measured as cytokine-induced activation, progressively declined with increasing concentrations of the tested antibodies, indicating effective inhibition of signaling through IL-6 ( A ), IL-17A ( B ), and the IL-17A/F heterodimer ( C ). Data were analyzed using nonlinear regression with a three-parameter dose–response model (log [inhibitor] vs. response), fitted using GraphPad Prism software. The curves shown represent a representative biological replicate performed with two technical replicates. The IC 50 values summarized in were calculated from three independent biological replicates.

    Journal: Antibodies

    Article Title: Development of Bispecific Antibody Targeting Human IL-17A and IL-6

    doi: 10.3390/antib15020029

    Figure Lengend Snippet: Neutralization potency of CPBT0853 targeting IL-17A ( A ) and IL-6, IL-17A. Representative graphs show IC 50 analysis performed using a reporter cell assay. For comparison, parental VHHs and monospecific referential antibodies were used. The cellular response, measured as cytokine-induced activation, progressively declined with increasing concentrations of the tested antibodies, indicating effective inhibition of signaling through IL-6 ( A ), IL-17A ( B ), and the IL-17A/F heterodimer ( C ). Data were analyzed using nonlinear regression with a three-parameter dose–response model (log [inhibitor] vs. response), fitted using GraphPad Prism software. The curves shown represent a representative biological replicate performed with two technical replicates. The IC 50 values summarized in were calculated from three independent biological replicates.

    Article Snippet: The binding of human, cynomolgus monkey ( Macaca fascicularis ), and mouse IL-6 and IL-17A (ACROBiosystems), human complex IL-17A/F (R&D System, Minneapolis, MN, USA) and human IL-17E and IL-17F (ACROBiosystems) to the anti-IL-6/anti-IL17A bispecific antibody CPBT0853 was analyzed using an Octet RED96 instrument (Sartorius AG).

    Techniques: Neutralization, Comparison, Activation Assay, Inhibition, Software

    Representative IC 50 curves showing inhibition of STATs phosphorylation in PBMCs stimulated with IL-6 and treated with increasing concentrations of the bispecific antibody CPBT0853. Phosphorylation of STAT1 ( A ) and STAT3 ( B ) was measured by flow cytometry. Data were normalized to cytokine-only controls and expressed as % pSTAT + lymphocytes. IC 50 values were calculated using a nonlinear regression with a three-parameter dose–response model (log [inhibitor] vs. response) in GraphPad Prism software. Each curve represents technical duplicates from PBMCs of one representative donor out of three tested.

    Journal: Antibodies

    Article Title: Development of Bispecific Antibody Targeting Human IL-17A and IL-6

    doi: 10.3390/antib15020029

    Figure Lengend Snippet: Representative IC 50 curves showing inhibition of STATs phosphorylation in PBMCs stimulated with IL-6 and treated with increasing concentrations of the bispecific antibody CPBT0853. Phosphorylation of STAT1 ( A ) and STAT3 ( B ) was measured by flow cytometry. Data were normalized to cytokine-only controls and expressed as % pSTAT + lymphocytes. IC 50 values were calculated using a nonlinear regression with a three-parameter dose–response model (log [inhibitor] vs. response) in GraphPad Prism software. Each curve represents technical duplicates from PBMCs of one representative donor out of three tested.

    Article Snippet: The binding of human, cynomolgus monkey ( Macaca fascicularis ), and mouse IL-6 and IL-17A (ACROBiosystems), human complex IL-17A/F (R&D System, Minneapolis, MN, USA) and human IL-17E and IL-17F (ACROBiosystems) to the anti-IL-6/anti-IL17A bispecific antibody CPBT0853 was analyzed using an Octet RED96 instrument (Sartorius AG).

    Techniques: Inhibition, Phospho-proteomics, Flow Cytometry, Software

    Inhibition of cytokine production (IL-6 and IL-8) in HFLS cells by CPBT0853. Levels of IL-6 ( A ) and IL-8 ( B ) secreted into the culture medium after stimulation of the cells with IL-17A. Additionally, cells were treated with bispecific and monospecific antibodies, as indicated. Data are shown as the mean ± SD from a minimum of four independent experiments. The bispecific antibody CPBT0853 effectively reduced the IL-6 and IL-8 levels, with higher efficiency, as compared to the monospecific antibodies, indicating enhanced anti-inflammatory activity. Additionally, the humanized IgG4 form of CPBT0853 (CPBT1269) was evaluated for comparison, showing activity in cytokine inhibition similar to that of the parental/original IgG1 form.

    Journal: Antibodies

    Article Title: Development of Bispecific Antibody Targeting Human IL-17A and IL-6

    doi: 10.3390/antib15020029

    Figure Lengend Snippet: Inhibition of cytokine production (IL-6 and IL-8) in HFLS cells by CPBT0853. Levels of IL-6 ( A ) and IL-8 ( B ) secreted into the culture medium after stimulation of the cells with IL-17A. Additionally, cells were treated with bispecific and monospecific antibodies, as indicated. Data are shown as the mean ± SD from a minimum of four independent experiments. The bispecific antibody CPBT0853 effectively reduced the IL-6 and IL-8 levels, with higher efficiency, as compared to the monospecific antibodies, indicating enhanced anti-inflammatory activity. Additionally, the humanized IgG4 form of CPBT0853 (CPBT1269) was evaluated for comparison, showing activity in cytokine inhibition similar to that of the parental/original IgG1 form.

    Article Snippet: The binding of human, cynomolgus monkey ( Macaca fascicularis ), and mouse IL-6 and IL-17A (ACROBiosystems), human complex IL-17A/F (R&D System, Minneapolis, MN, USA) and human IL-17E and IL-17F (ACROBiosystems) to the anti-IL-6/anti-IL17A bispecific antibody CPBT0853 was analyzed using an Octet RED96 instrument (Sartorius AG).

    Techniques: Inhibition, Activity Assay, Comparison

    To model EA or MGA respectively, Balb/c or Il4ra -/- mice were given five intranasal (i.n.) challenges with 100ug house dust mite (HDM) extract every week (followed by two days resting) for three consecutive weeks. A final i.n. HDM challenge was given 24 hours prior to harvest. ( A ) Lung sections were stained and representative Masson trichrome (collagen), α-smooth muscle actin (αSMA), and hematoxylin and eosin (H&E) sections and accompanying quantifications are shown. ( B ) Airway resistance to increasing doses of methacholine exposure (6-8 mice per group). (C) Expression of mRNA for IL13 and IL17, assessed by quantitative PCR analyses of lung samples. mRNA expression was calculated relative to GAPDH for 5 mice per group. ( D ) Number of neutrophils or eosinophils in the left lung lobe of EA or MGA induced mice, as assessed by flow cytometry. ( E ) MGA-induced animals were treated with 50ug dexamethasone intratracheally one hour prior to each allergen challenge, beginning on day 7. Lung sections were stained and representative Masson trichrome and αSMA sections and accompanying quantifications are shown. ( F ) Number of neutrophils or eosinophils in the left lung lobe of MGA induced mice treated with or without dexamethasone, as assessed by flow cytometry. ( G ) MGA-induced animals were treated with 100ug anti-IL17A or matching isotype control i.p. beginning on day 7 and continuing every other day until harvest. Lung sections were stained, and representative H&E sections and accompanying quantifications are shown. Trichrome data show area of interest values covering full lung section of 6 individual mice per condition. αSMA data show mean values of all bronchi scored from 6 mice per condition. Data are representative of 3 independent experiments. *P < 0.05, **P < 0.005, ***P < 0.0005, ****P < 0.00005; HPF, high-power field; ns, nonsignificant.

    Journal: bioRxiv

    Article Title: The metabolic reprogramming of T cells controls airway remodeling in severe asthma

    doi: 10.64898/2026.03.19.712985

    Figure Lengend Snippet: To model EA or MGA respectively, Balb/c or Il4ra -/- mice were given five intranasal (i.n.) challenges with 100ug house dust mite (HDM) extract every week (followed by two days resting) for three consecutive weeks. A final i.n. HDM challenge was given 24 hours prior to harvest. ( A ) Lung sections were stained and representative Masson trichrome (collagen), α-smooth muscle actin (αSMA), and hematoxylin and eosin (H&E) sections and accompanying quantifications are shown. ( B ) Airway resistance to increasing doses of methacholine exposure (6-8 mice per group). (C) Expression of mRNA for IL13 and IL17, assessed by quantitative PCR analyses of lung samples. mRNA expression was calculated relative to GAPDH for 5 mice per group. ( D ) Number of neutrophils or eosinophils in the left lung lobe of EA or MGA induced mice, as assessed by flow cytometry. ( E ) MGA-induced animals were treated with 50ug dexamethasone intratracheally one hour prior to each allergen challenge, beginning on day 7. Lung sections were stained and representative Masson trichrome and αSMA sections and accompanying quantifications are shown. ( F ) Number of neutrophils or eosinophils in the left lung lobe of MGA induced mice treated with or without dexamethasone, as assessed by flow cytometry. ( G ) MGA-induced animals were treated with 100ug anti-IL17A or matching isotype control i.p. beginning on day 7 and continuing every other day until harvest. Lung sections were stained, and representative H&E sections and accompanying quantifications are shown. Trichrome data show area of interest values covering full lung section of 6 individual mice per condition. αSMA data show mean values of all bronchi scored from 6 mice per condition. Data are representative of 3 independent experiments. *P < 0.05, **P < 0.005, ***P < 0.0005, ****P < 0.00005; HPF, high-power field; ns, nonsignificant.

    Article Snippet: To block IL-17 signaling, 100ug anti-IL17A (17F3; BioXCell) or matching isotype control (MOPC-21; BioXCell) were given intraperitoneally (i.p.) to HDM induced Ilr4a -/- mice beginning on day 7 and continuing every other day for a total of 7 injections.

    Techniques: Staining, Expressing, Real-time Polymerase Chain Reaction, Flow Cytometry, Control

    Antagonizing IL-17A significantly reduces oxidative stress production in whole blood of C57BL/6J mice treated with Ang II over one week, attenuates vascular inflammation based on a trend, and has no impact on vascular dysfunction development. ( A ) Acetylcholine induced vascular relaxation in C57BL/6J mice, in C57BL/6J + Ang II mice, and in C57BL/6J + Ang II mice treated with either 60 µg/g bodyweight of an anti-IL17A or isotype control antibody over one week, n = 3–8 mice per group based on two independent experiments, two-way ANOVA with Bonferroni multiple comparison test. Black stars show the significancy between C57BL/6J and C57BL/6J + Ang II + ISO treated mice. Blue stars demonstrate the significancy between C57BL/6J versus C57BL/6J + Ang II + anti-IL17A treated mice. Black ### show the significancy between C57BL/6J and C57BL/6J + Ang II treated mice. (**/## p ≤ 0.01; ***/### p < 0.001). ( B ) ROS/RNS measurement in whole blood after 10 min of PDBu stimulation. Partially repeated measurements of pooled samples, n = 6–7 mice per group based on two independent experiments, one-way ANOVA with Bonferroni’s posttest. ( C ) Aortic inflammation detected via flow cytometry (gating strategy as described in ), n = 6–8 mice per group based on independent experiments, Kruskal–Wallis one-way ANOVA with Dunn’s posttest. All data are shown as the mean ± SEM. * p ≤ 0.05, ** p ≤ 0.01.

    Journal: Antioxidants

    Article Title: Antagonizing IL-17A Reduces Vascular Inflammation and Attenuates Oxidative Stress Formation but Does Not Significantly Improve Vascular Dysfunction Induced by One Week of Angiotensin II Treatment

    doi: 10.3390/antiox15020229

    Figure Lengend Snippet: Antagonizing IL-17A significantly reduces oxidative stress production in whole blood of C57BL/6J mice treated with Ang II over one week, attenuates vascular inflammation based on a trend, and has no impact on vascular dysfunction development. ( A ) Acetylcholine induced vascular relaxation in C57BL/6J mice, in C57BL/6J + Ang II mice, and in C57BL/6J + Ang II mice treated with either 60 µg/g bodyweight of an anti-IL17A or isotype control antibody over one week, n = 3–8 mice per group based on two independent experiments, two-way ANOVA with Bonferroni multiple comparison test. Black stars show the significancy between C57BL/6J and C57BL/6J + Ang II + ISO treated mice. Blue stars demonstrate the significancy between C57BL/6J versus C57BL/6J + Ang II + anti-IL17A treated mice. Black ### show the significancy between C57BL/6J and C57BL/6J + Ang II treated mice. (**/## p ≤ 0.01; ***/### p < 0.001). ( B ) ROS/RNS measurement in whole blood after 10 min of PDBu stimulation. Partially repeated measurements of pooled samples, n = 6–7 mice per group based on two independent experiments, one-way ANOVA with Bonferroni’s posttest. ( C ) Aortic inflammation detected via flow cytometry (gating strategy as described in ), n = 6–8 mice per group based on independent experiments, Kruskal–Wallis one-way ANOVA with Dunn’s posttest. All data are shown as the mean ± SEM. * p ≤ 0.05, ** p ≤ 0.01.

    Article Snippet: Novartis only provide the anti-IL17A antibody.

    Techniques: Control, Comparison, Flow Cytometry

    Memory versus naïve T cell responses following CLP. Twenty-four hrs. following sham procedure or CLP in C57Bl/6 mice, T cell cytokine production in response to in vitro T cell receptor stimulation were assessed. A Percentage of memory (CD44 + /CD11 + ) and naïve (CD44 − /CD11a − ) splenic (Left) or hepatic (Right) CD4 (Top) and CD8 (Bottom) T cells producing IFNγ, IL2, IL17A or TNF. Gating: FSC/SSC, Singlets, Live, CD90/CD4 or CD90/CD8, CD44/CD11a, IFNγ, IL2, IL17A or TNF. IL17A numbers displayed graphically following multiplication by 10 for clarity. Comparisons made by two-way ANOVA comparing CLP/Sham and Memory/Naïve. * = p < 0.05 for interaction effect, # = p < 0.05 for CLP effect, ^ = p < 0.05 for Memory effect. Analyzed by 2-way ANOVA. Figures representative of 2 independent experiments. N = 3/group. B Pie graphs demonstrating the percentage of splenic memory (CD44 + /CD11 + ) and naïve (CD44 − /CD11a − ) CD4 and CD8 T cells producing one cytokine (Red), two cytokines (Blue), or three cytokines (Yellow) in response to in vitro T cell receptor stimulation. CD4 and CD8 T cell responses analyzed separately by 3-way ANOVA. N = 3/group. Gating: FSC/SSC, Singlets, Live Cells, CD90/CD4 or CD90/CD8, IFNγ, IL2, or TNF

    Journal: Molecular Medicine

    Article Title: IL17F + naïve and IFNγ + memory CD8 T cells drive hepatic dysfunction in the cecal ligation and puncture model of sepsis

    doi: 10.1186/s10020-025-01411-2

    Figure Lengend Snippet: Memory versus naïve T cell responses following CLP. Twenty-four hrs. following sham procedure or CLP in C57Bl/6 mice, T cell cytokine production in response to in vitro T cell receptor stimulation were assessed. A Percentage of memory (CD44 + /CD11 + ) and naïve (CD44 − /CD11a − ) splenic (Left) or hepatic (Right) CD4 (Top) and CD8 (Bottom) T cells producing IFNγ, IL2, IL17A or TNF. Gating: FSC/SSC, Singlets, Live, CD90/CD4 or CD90/CD8, CD44/CD11a, IFNγ, IL2, IL17A or TNF. IL17A numbers displayed graphically following multiplication by 10 for clarity. Comparisons made by two-way ANOVA comparing CLP/Sham and Memory/Naïve. * = p < 0.05 for interaction effect, # = p < 0.05 for CLP effect, ^ = p < 0.05 for Memory effect. Analyzed by 2-way ANOVA. Figures representative of 2 independent experiments. N = 3/group. B Pie graphs demonstrating the percentage of splenic memory (CD44 + /CD11 + ) and naïve (CD44 − /CD11a − ) CD4 and CD8 T cells producing one cytokine (Red), two cytokines (Blue), or three cytokines (Yellow) in response to in vitro T cell receptor stimulation. CD4 and CD8 T cell responses analyzed separately by 3-way ANOVA. N = 3/group. Gating: FSC/SSC, Singlets, Live Cells, CD90/CD4 or CD90/CD8, IFNγ, IL2, or TNF

    Article Snippet: IFNγ (XMG1.2, dose: 0.5 mg), IL12p40 (C17.8, dose: 1 mg), TNF (XT3.11, 1 mg), IL17A (17F3, dose: 0.5 mg) and IL17F (MM17F8F5.1A9, dose: 0.5 mg) blocking antibodies were all obtained from BioXCell (Lebanon, NH), diluted from stock concentration in sterile PBS and administered through intraperitoneal injection at in vivo blocking doses as previously described in the literature. (Jordan et al. ; Taylor et al. ; Naik et al. ; Lemaire et al. ).

    Techniques: In Vitro

    Effects of Immune Education and Specific Cytokine Blockade on the Serum Cytokine Response to CLP. Immune Educated or Control C57Bl/6 mice were sacrificed 24 h. following CLP with or without cytokine blockade. A Depiction of experimental design. B-G Serum levels of ( B ) IFNγ, C IL12p40, D IL17, E TNF, F IL1β and ( G ) IL6. Analyzed by 2-way ANOVA with Log10 transformation if data failed normality for all CLP groups. * = p < 0.05 for comparisons between two groups, # = p < 0.05 for an effect of cytokine blockade on the CLP response compared to untreated CLP. Baseline excluded from statistical analysis. N = 4–13/group

    Journal: Molecular Medicine

    Article Title: IL17F + naïve and IFNγ + memory CD8 T cells drive hepatic dysfunction in the cecal ligation and puncture model of sepsis

    doi: 10.1186/s10020-025-01411-2

    Figure Lengend Snippet: Effects of Immune Education and Specific Cytokine Blockade on the Serum Cytokine Response to CLP. Immune Educated or Control C57Bl/6 mice were sacrificed 24 h. following CLP with or without cytokine blockade. A Depiction of experimental design. B-G Serum levels of ( B ) IFNγ, C IL12p40, D IL17, E TNF, F IL1β and ( G ) IL6. Analyzed by 2-way ANOVA with Log10 transformation if data failed normality for all CLP groups. * = p < 0.05 for comparisons between two groups, # = p < 0.05 for an effect of cytokine blockade on the CLP response compared to untreated CLP. Baseline excluded from statistical analysis. N = 4–13/group

    Article Snippet: IFNγ (XMG1.2, dose: 0.5 mg), IL12p40 (C17.8, dose: 1 mg), TNF (XT3.11, 1 mg), IL17A (17F3, dose: 0.5 mg) and IL17F (MM17F8F5.1A9, dose: 0.5 mg) blocking antibodies were all obtained from BioXCell (Lebanon, NH), diluted from stock concentration in sterile PBS and administered through intraperitoneal injection at in vivo blocking doses as previously described in the literature. (Jordan et al. ; Taylor et al. ; Naik et al. ; Lemaire et al. ).

    Techniques: Control, Transformation Assay

    Effects of Immune Education, CLP, and Specific Cytokine Blockade on T cell Cytokine Production. A-C Immune Educated or Control IFNγ-eYFP reporter mice on a C57Bl/6 background were sacrificed prior to or 24 h. following CLP. IFNγ + T cells were assessed. Percent IFNγ + CD4 (Left) and CD8 (Right) T cells in the ( A ) spleen and ( B ) liver. C Histograms of IFNγ + (Red) and negative (Gray) splenic CD4 T cells in Educated mice following CLP. D-E Immune Educated or Control IL17A EGFP /IL17F mCherry reporter mice on a C57Bl/6 background were sacrificed prior to or 24 h. following CLP. IL17A + and IL17F + T cells were assessed. Percent IL17A + CD4 (Left), IL17A + CD8 (Middle Left), IL17F + CD4 (Middle Right) and IL17F + CD8 (Right) T cells in the ( D ) inguinal lymph node (ILN) and ( E ) liver. F Histograms of IL17A + (Orange) vs IL17F + (Green) ILN CD4 T cells in Educated mice following CLP. A-F * = p < 0.05 for comparisons between two groups, † = p < 0.05 for interaction effect, # = p < 0.05 for CLP effect, ^ = p < 0.05 for Education effect. N = 3–4/group. G Hepatic leukocytes were isolated from Educated or control C57Bl/6 mice prior to or 24 h. following CLP alone or with specific cytokine blockade and intracellular cytokine production was assessed following in vitro PMA/Ionomycin stimulation. Percent IFNγ + (Left) and IL17A + (Right) CD8 T cells. Analyzed by 2-way ANOVA. * = p < 0.05 for comparisons between two groups, # = p < 0.05 for specific cytokine effect, p values for interactions, effect of education or effect of blockade displayed. N = 3–5/group. Gating: FSC/SSC, Singlets, Live, CD90/CD4 or CD90/CD8, eYFP, eGFP, mCherry, IFNγ, IL17A, or TNF

    Journal: Molecular Medicine

    Article Title: IL17F + naïve and IFNγ + memory CD8 T cells drive hepatic dysfunction in the cecal ligation and puncture model of sepsis

    doi: 10.1186/s10020-025-01411-2

    Figure Lengend Snippet: Effects of Immune Education, CLP, and Specific Cytokine Blockade on T cell Cytokine Production. A-C Immune Educated or Control IFNγ-eYFP reporter mice on a C57Bl/6 background were sacrificed prior to or 24 h. following CLP. IFNγ + T cells were assessed. Percent IFNγ + CD4 (Left) and CD8 (Right) T cells in the ( A ) spleen and ( B ) liver. C Histograms of IFNγ + (Red) and negative (Gray) splenic CD4 T cells in Educated mice following CLP. D-E Immune Educated or Control IL17A EGFP /IL17F mCherry reporter mice on a C57Bl/6 background were sacrificed prior to or 24 h. following CLP. IL17A + and IL17F + T cells were assessed. Percent IL17A + CD4 (Left), IL17A + CD8 (Middle Left), IL17F + CD4 (Middle Right) and IL17F + CD8 (Right) T cells in the ( D ) inguinal lymph node (ILN) and ( E ) liver. F Histograms of IL17A + (Orange) vs IL17F + (Green) ILN CD4 T cells in Educated mice following CLP. A-F * = p < 0.05 for comparisons between two groups, † = p < 0.05 for interaction effect, # = p < 0.05 for CLP effect, ^ = p < 0.05 for Education effect. N = 3–4/group. G Hepatic leukocytes were isolated from Educated or control C57Bl/6 mice prior to or 24 h. following CLP alone or with specific cytokine blockade and intracellular cytokine production was assessed following in vitro PMA/Ionomycin stimulation. Percent IFNγ + (Left) and IL17A + (Right) CD8 T cells. Analyzed by 2-way ANOVA. * = p < 0.05 for comparisons between two groups, # = p < 0.05 for specific cytokine effect, p values for interactions, effect of education or effect of blockade displayed. N = 3–5/group. Gating: FSC/SSC, Singlets, Live, CD90/CD4 or CD90/CD8, eYFP, eGFP, mCherry, IFNγ, IL17A, or TNF

    Article Snippet: IFNγ (XMG1.2, dose: 0.5 mg), IL12p40 (C17.8, dose: 1 mg), TNF (XT3.11, 1 mg), IL17A (17F3, dose: 0.5 mg) and IL17F (MM17F8F5.1A9, dose: 0.5 mg) blocking antibodies were all obtained from BioXCell (Lebanon, NH), diluted from stock concentration in sterile PBS and administered through intraperitoneal injection at in vivo blocking doses as previously described in the literature. (Jordan et al. ; Taylor et al. ; Naik et al. ; Lemaire et al. ).

    Techniques: Control, Isolation, In Vitro

    Effects of Immune Education, CLP, and Specific Cytokine Blockade on Innate and T Cell Immune Responses. Hepatic leukocytes were isolated from Educated or control C57Bl/6 mice prior to or 24 h. following CLP alone or with specific cytokine blockade; innate immune cell numbers and cytokine production were assessed. Total number of hepatic neutrophils ( A ) or MoDCs ( B ), and percent TNF + ( C ), IL1β + ( D ) or IL12p40 + MoDCs ( E ) and total number of hepatic CD8 T cells ( F ) in control (Blue) or Educated (Red) mice at baseline, following CLP or following CLP with IFNγ, IL12p40, TNF, or IL17A/F combined blockade. CLP with IL17A or IL17F blockade shown to the right. Analyzed by 2-way ANOVA. IL17A and IL17F analyzed separately. * = p < 0.05, ** = p < 0.01, *** = p < 0.001, **** = p < 0.0001 for comparisons between two groups, # = p < 0.05 for cytokine effect compared to CLP. N = 3–12/group. Cytokine production analyzed in a subset of samples. Gating: Neutrophils = FSC/SSC, Singlets, Live Cells, CD11b + /CD11c − , Ly6G + /Ly6C + , MoDCs = FSC/SSC, Singlets, Live, CD11b + /CD11c − , Ly6G − , MHCII + , Macrophages = FSC/SSC, Singlets, Live, CD11b + /CD11c − , Ly6G − , MHCII − , Ly6C Hi /CD64 + , CD8 + T cells = FSC/SSC, Singlets, Live, CD90 + /CD8 +

    Journal: Molecular Medicine

    Article Title: IL17F + naïve and IFNγ + memory CD8 T cells drive hepatic dysfunction in the cecal ligation and puncture model of sepsis

    doi: 10.1186/s10020-025-01411-2

    Figure Lengend Snippet: Effects of Immune Education, CLP, and Specific Cytokine Blockade on Innate and T Cell Immune Responses. Hepatic leukocytes were isolated from Educated or control C57Bl/6 mice prior to or 24 h. following CLP alone or with specific cytokine blockade; innate immune cell numbers and cytokine production were assessed. Total number of hepatic neutrophils ( A ) or MoDCs ( B ), and percent TNF + ( C ), IL1β + ( D ) or IL12p40 + MoDCs ( E ) and total number of hepatic CD8 T cells ( F ) in control (Blue) or Educated (Red) mice at baseline, following CLP or following CLP with IFNγ, IL12p40, TNF, or IL17A/F combined blockade. CLP with IL17A or IL17F blockade shown to the right. Analyzed by 2-way ANOVA. IL17A and IL17F analyzed separately. * = p < 0.05, ** = p < 0.01, *** = p < 0.001, **** = p < 0.0001 for comparisons between two groups, # = p < 0.05 for cytokine effect compared to CLP. N = 3–12/group. Cytokine production analyzed in a subset of samples. Gating: Neutrophils = FSC/SSC, Singlets, Live Cells, CD11b + /CD11c − , Ly6G + /Ly6C + , MoDCs = FSC/SSC, Singlets, Live, CD11b + /CD11c − , Ly6G − , MHCII + , Macrophages = FSC/SSC, Singlets, Live, CD11b + /CD11c − , Ly6G − , MHCII − , Ly6C Hi /CD64 + , CD8 + T cells = FSC/SSC, Singlets, Live, CD90 + /CD8 +

    Article Snippet: IFNγ (XMG1.2, dose: 0.5 mg), IL12p40 (C17.8, dose: 1 mg), TNF (XT3.11, 1 mg), IL17A (17F3, dose: 0.5 mg) and IL17F (MM17F8F5.1A9, dose: 0.5 mg) blocking antibodies were all obtained from BioXCell (Lebanon, NH), diluted from stock concentration in sterile PBS and administered through intraperitoneal injection at in vivo blocking doses as previously described in the literature. (Jordan et al. ; Taylor et al. ; Naik et al. ; Lemaire et al. ).

    Techniques: Isolation, Control

    Effects of Immune Education, CLP, and Specific Cytokine Blockade on CLP-Induced Hepatic Dysfunction. Immune Educated (Red) or Control (Blue) C57Bl/6 mice were sacrificed prior to or 24 h. following CLP alone or with cytokine blockade. A Hepatic tissue was assessed by RT-PCR for log 10 transformed relative transcription levels of SCLO1a1, SLC10, and ABCC2. B Serum Alanine aminotransferase (ALT). C Log 10 transformed peritoneal bacterial colony forming units. D Probability of Survival in the days following CLP with blockade as noted. Data as mean ± SD. Analyzed by 2-way ANOVA. * = p < 0.05 for comparisons between two groups. P Int = Significant Interaction between Blockade and Education, P Block = Significant Effect of Treatment (CLP + antibody blockade), P Edu = Significant Effect of Control vs Immune Education. For A , primary 2-way ANOVA comparison between Baseline, CLP, CLP + αIFNγ, CLP + αIL12p40, CLP + αTNF, and CLP + αIL17A/F. IL17A and IL17F blockade compared to each other separately from other comparisons. Survival analyzed by Log-rank Test. N = 4–22/group

    Journal: Molecular Medicine

    Article Title: IL17F + naïve and IFNγ + memory CD8 T cells drive hepatic dysfunction in the cecal ligation and puncture model of sepsis

    doi: 10.1186/s10020-025-01411-2

    Figure Lengend Snippet: Effects of Immune Education, CLP, and Specific Cytokine Blockade on CLP-Induced Hepatic Dysfunction. Immune Educated (Red) or Control (Blue) C57Bl/6 mice were sacrificed prior to or 24 h. following CLP alone or with cytokine blockade. A Hepatic tissue was assessed by RT-PCR for log 10 transformed relative transcription levels of SCLO1a1, SLC10, and ABCC2. B Serum Alanine aminotransferase (ALT). C Log 10 transformed peritoneal bacterial colony forming units. D Probability of Survival in the days following CLP with blockade as noted. Data as mean ± SD. Analyzed by 2-way ANOVA. * = p < 0.05 for comparisons between two groups. P Int = Significant Interaction between Blockade and Education, P Block = Significant Effect of Treatment (CLP + antibody blockade), P Edu = Significant Effect of Control vs Immune Education. For A , primary 2-way ANOVA comparison between Baseline, CLP, CLP + αIFNγ, CLP + αIL12p40, CLP + αTNF, and CLP + αIL17A/F. IL17A and IL17F blockade compared to each other separately from other comparisons. Survival analyzed by Log-rank Test. N = 4–22/group

    Article Snippet: IFNγ (XMG1.2, dose: 0.5 mg), IL12p40 (C17.8, dose: 1 mg), TNF (XT3.11, 1 mg), IL17A (17F3, dose: 0.5 mg) and IL17F (MM17F8F5.1A9, dose: 0.5 mg) blocking antibodies were all obtained from BioXCell (Lebanon, NH), diluted from stock concentration in sterile PBS and administered through intraperitoneal injection at in vivo blocking doses as previously described in the literature. (Jordan et al. ; Taylor et al. ; Naik et al. ; Lemaire et al. ).

    Techniques: Control, Reverse Transcription Polymerase Chain Reaction, Transformation Assay, Blocking Assay, Comparison

    Effects of CLP on Pet Shop and SPF J:ARC(S) Swiss Outbred Mice. Pet Store or Control J:ARC(S) Swiss Outbred mice were sacrificed 24 h. following CLP. A Serum levels of IFNγ, IL12p40, and IL17. B Total number of hepatic neutrophils, MoDCs, or cDCs. C RT-PCR log 10 transformed relative transcription levels of SCLO1a1 from hepatic tissue, serum alanine aminotransferase (ALT), and log 10 transformed peritoneal bacterial colony forming units. Analyzed by 2-way ANOVA. P Int = Significant Interaction between Blockade and Pet Store/Laboratory, P Block = Significant Effect of Treatment (CLP + antibody blockade), P group = Significant Effect of Pet Store/Laboratory Strain. 2-way ANOVA comparison between Baseline, CLP, CLP + αIFNγ, and CLP + αIL17F. * = p < 0.05 for comparisons between two groups. N = 4–7/group. Gating: Neutrophils = FSC/SSC, Singlets, Live, CD11b + /CD11c − , Ly6G + /Ly6C + , MoDCs = FSC/SSC, Singlets, Live, CD11b + /CD11c − , Ly6G − , MHCII + , cDCs = FSC/SSC, Singlets, Live, CD11c + , MHCII +

    Journal: Molecular Medicine

    Article Title: IL17F + naïve and IFNγ + memory CD8 T cells drive hepatic dysfunction in the cecal ligation and puncture model of sepsis

    doi: 10.1186/s10020-025-01411-2

    Figure Lengend Snippet: Effects of CLP on Pet Shop and SPF J:ARC(S) Swiss Outbred Mice. Pet Store or Control J:ARC(S) Swiss Outbred mice were sacrificed 24 h. following CLP. A Serum levels of IFNγ, IL12p40, and IL17. B Total number of hepatic neutrophils, MoDCs, or cDCs. C RT-PCR log 10 transformed relative transcription levels of SCLO1a1 from hepatic tissue, serum alanine aminotransferase (ALT), and log 10 transformed peritoneal bacterial colony forming units. Analyzed by 2-way ANOVA. P Int = Significant Interaction between Blockade and Pet Store/Laboratory, P Block = Significant Effect of Treatment (CLP + antibody blockade), P group = Significant Effect of Pet Store/Laboratory Strain. 2-way ANOVA comparison between Baseline, CLP, CLP + αIFNγ, and CLP + αIL17F. * = p < 0.05 for comparisons between two groups. N = 4–7/group. Gating: Neutrophils = FSC/SSC, Singlets, Live, CD11b + /CD11c − , Ly6G + /Ly6C + , MoDCs = FSC/SSC, Singlets, Live, CD11b + /CD11c − , Ly6G − , MHCII + , cDCs = FSC/SSC, Singlets, Live, CD11c + , MHCII +

    Article Snippet: IFNγ (XMG1.2, dose: 0.5 mg), IL12p40 (C17.8, dose: 1 mg), TNF (XT3.11, 1 mg), IL17A (17F3, dose: 0.5 mg) and IL17F (MM17F8F5.1A9, dose: 0.5 mg) blocking antibodies were all obtained from BioXCell (Lebanon, NH), diluted from stock concentration in sterile PBS and administered through intraperitoneal injection at in vivo blocking doses as previously described in the literature. (Jordan et al. ; Taylor et al. ; Naik et al. ; Lemaire et al. ).

    Techniques: Control, Reverse Transcription Polymerase Chain Reaction, Transformation Assay, Blocking Assay, Comparison