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Bio X Cell anti il 12β antibody treatment
Cardiac <t>IL-12β</t> expression was significantly increased after TAC. (A) Western blots and quantified data of LV IL-12β expression in WT sham and WT TAC mice. (B) Representative LV IL-12β staining images and quantified data of IL-12β + area. (C) Representative images of IL-12β and CD45 co-immunostaining of WT mice LV tissue under sham and TAC conditions. The green stain in panel B is due to cardiac autofluorescence recorded at FITC channel. ∗p < 0.05; n = 5 per group.
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Bio X Cell anti b7 h3 antibody treatment group
Cardiac <t>IL-12β</t> expression was significantly increased after TAC. (A) Western blots and quantified data of LV IL-12β expression in WT sham and WT TAC mice. (B) Representative LV IL-12β staining images and quantified data of IL-12β + area. (C) Representative images of IL-12β and CD45 co-immunostaining of WT mice LV tissue under sham and TAC conditions. The green stain in panel B is due to cardiac autofluorescence recorded at FITC channel. ∗p < 0.05; n = 5 per group.
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Image Search Results


Therapeutic neutralization of TSLP protects against AAA development. (A) Schematic diagram of the experimental protocol for anti-mouse TSLP antibody (anti-TSLP) administration in the PPE-induced AAA model. (B) Comparison of the maximum abdominal aortic diameter in normal saline-treated and TSLP-treated mice at day 14 (n=6 mice per group). (C, D) Representative histological staining and corresponding quantification for Elastica Van Gieson (EVG) (n=6 mice per group). (E–J) Representative images and quantitative analysis of immunohistochemical staining for CD68 (E, F) , MMP2 (G, H) and MMP9 (I, J) expression in the aortic wall. Positive areas are presented as a percentage of the total area (n=6 mice per group). Scale bars: (A) 1mm; (C) 500 μm; (E, G, I) 200 μm (top), 50 μm (bottom). All quantitative data are presented as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001 (unpaired two-tailed Student’s t-test). Ctrl, control. Red arrows indicate representative positive staining areas.

Journal: Frontiers in Immunology

Article Title: Thymic stromal lymphopoietin promotes abdominal aortic aneurysm formation by regulating macrophage polarization

doi: 10.3389/fimmu.2026.1767913

Figure Lengend Snippet: Therapeutic neutralization of TSLP protects against AAA development. (A) Schematic diagram of the experimental protocol for anti-mouse TSLP antibody (anti-TSLP) administration in the PPE-induced AAA model. (B) Comparison of the maximum abdominal aortic diameter in normal saline-treated and TSLP-treated mice at day 14 (n=6 mice per group). (C, D) Representative histological staining and corresponding quantification for Elastica Van Gieson (EVG) (n=6 mice per group). (E–J) Representative images and quantitative analysis of immunohistochemical staining for CD68 (E, F) , MMP2 (G, H) and MMP9 (I, J) expression in the aortic wall. Positive areas are presented as a percentage of the total area (n=6 mice per group). Scale bars: (A) 1mm; (C) 500 μm; (E, G, I) 200 μm (top), 50 μm (bottom). All quantitative data are presented as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001 (unpaired two-tailed Student’s t-test). Ctrl, control. Red arrows indicate representative positive staining areas.

Article Snippet: Anti-TSLP antibody treatment: Anti-TSLP antibody (HY-P990150, MCE, USA) was administered via intraperitoneal injection starting on day 1 after PPE induction at a dose of 20 mg/kg, and then every other day thereafter.

Techniques: Neutralization, Comparison, Saline, Staining, Immunohistochemical staining, Expressing, Two Tailed Test, Control

Schematic illustration of PTR-SeNPs and MUC1@PTR-SeNPs synthesis and their anti-tumor efficacy against human triple-negative breast cancer.

Journal: Bioactive Materials

Article Title: Translational selenium nanoparticles trigger apoptosis in triple-negative breast cancer cells through the MAPKs/Bcl2 pathway

doi: 10.1016/j.bioactmat.2026.02.027

Figure Lengend Snippet: Schematic illustration of PTR-SeNPs and MUC1@PTR-SeNPs synthesis and their anti-tumor efficacy against human triple-negative breast cancer.

Article Snippet: Anti-human MUC1 therapeutic antibody Fab fragment (7B8) were purchased From Creative Biolabs (TAB-423MZ-F, USA).

Techniques:

Structure characterization of PTR-SeNPs and MUC1@ PTR-SeNPs. Structure characterization of PTR-SeNPs by (A) TEM, (B) Zetasizer Nano ZS, (C, D) Nanosight NS300, (E1-4) HRTEM-EDS and (F, G) FT-IR. (H) Confirmation of MUC1-C + PTR-SeNPs conjugation by confocal microscopy after fluorescent labeling with anti-mouse IgG (H + L). (I, J) Characterization results of the particle size and potential of MUC1@PTR-SeNPs

Journal: Bioactive Materials

Article Title: Translational selenium nanoparticles trigger apoptosis in triple-negative breast cancer cells through the MAPKs/Bcl2 pathway

doi: 10.1016/j.bioactmat.2026.02.027

Figure Lengend Snippet: Structure characterization of PTR-SeNPs and MUC1@ PTR-SeNPs. Structure characterization of PTR-SeNPs by (A) TEM, (B) Zetasizer Nano ZS, (C, D) Nanosight NS300, (E1-4) HRTEM-EDS and (F, G) FT-IR. (H) Confirmation of MUC1-C + PTR-SeNPs conjugation by confocal microscopy after fluorescent labeling with anti-mouse IgG (H + L). (I, J) Characterization results of the particle size and potential of MUC1@PTR-SeNPs

Article Snippet: Anti-human MUC1 therapeutic antibody Fab fragment (7B8) were purchased From Creative Biolabs (TAB-423MZ-F, USA).

Techniques: Conjugation Assay, Confocal Microscopy, Labeling

In vitro anti-tumor efficacy of PTR-SeNPs and MUC1@PTR-SeNPs on 17 TNBC c ell lines. ( A, B ) Protein expression level of MUC1 in 17 different TNBC cell lines. ( C, D ) IC 50 and maximum % growth inhibition of PTR-SeNPs and MUC1@PTR-SeNPs on 17 TNBC cell lines. ( E, G ) Cell cycle distribution triggered by PTR-SeNPs and MUC1@PTR-SeNPs in HCC1937 and MDA-MB-436 cells. After treatment with PTR-SeNPs or MUC1@PTR-SeNPs (4 and 40 μM) in HCC1937 and MDA-MB-436 cells for 72 h, cells were stained with propidium iodide followed by flow cytometry analysis using MultiCycle software. The apoptotic cell death was quantified by measuring the sub-G1 cell population. ( F, H ) Phosphatidylserine translocation mediated by PTR-SeNPs and MUC1@PTR-SeNPs in HCC1937 and MDA-MB-436 cells. After treatment with MUC1@PTR-SeNPs (4 and 40 μM) for 48 h, cells were co-stained with propidium iodide and Annexin-V-FITC followed by flow cytometry analysis [early apoptotic subset: Annexin V+/PI- (green); late apoptotic subset: Annexin V+/PT+ (red)].

Journal: Bioactive Materials

Article Title: Translational selenium nanoparticles trigger apoptosis in triple-negative breast cancer cells through the MAPKs/Bcl2 pathway

doi: 10.1016/j.bioactmat.2026.02.027

Figure Lengend Snippet: In vitro anti-tumor efficacy of PTR-SeNPs and MUC1@PTR-SeNPs on 17 TNBC c ell lines. ( A, B ) Protein expression level of MUC1 in 17 different TNBC cell lines. ( C, D ) IC 50 and maximum % growth inhibition of PTR-SeNPs and MUC1@PTR-SeNPs on 17 TNBC cell lines. ( E, G ) Cell cycle distribution triggered by PTR-SeNPs and MUC1@PTR-SeNPs in HCC1937 and MDA-MB-436 cells. After treatment with PTR-SeNPs or MUC1@PTR-SeNPs (4 and 40 μM) in HCC1937 and MDA-MB-436 cells for 72 h, cells were stained with propidium iodide followed by flow cytometry analysis using MultiCycle software. The apoptotic cell death was quantified by measuring the sub-G1 cell population. ( F, H ) Phosphatidylserine translocation mediated by PTR-SeNPs and MUC1@PTR-SeNPs in HCC1937 and MDA-MB-436 cells. After treatment with MUC1@PTR-SeNPs (4 and 40 μM) for 48 h, cells were co-stained with propidium iodide and Annexin-V-FITC followed by flow cytometry analysis [early apoptotic subset: Annexin V+/PI- (green); late apoptotic subset: Annexin V+/PT+ (red)].

Article Snippet: Anti-human MUC1 therapeutic antibody Fab fragment (7B8) were purchased From Creative Biolabs (TAB-423MZ-F, USA).

Techniques: In Vitro, Expressing, Inhibition, Staining, Flow Cytometry, Software, Translocation Assay

In vivo anti-tumor efficacy of MUC1@PTR- SeNPs. (A) MUC1 mRNA expression in normal tissue and primary breast cancer tumor using GEPIA database. ( B ) MUC1 expression in tumor tissues of MDA-MB-468-bearing mice in preliminary study. (C – E) Dose-dependent study of tumor inhibition effect of MUC1@PTR-SeNPs [75 (Low), 375 (Mid) & 750 μg (High) Se/kg BW/day] on BALB/c nude mice transplanted with MDA-MB-468 xenograft after oral administration for 30 days. PTR-SeNPs (High; 750 μg Se/kg BW/day) was used to investigate the possible improvement of in vivo anti-tumor efficacy by the MUC1@PTR-SeNPs. Quantitative analysis of Se content (μg/g) in (F) blood and (G) tumor tissue of experimental mice. (H) H&E, Ki67 and Tunnel fluorescence staining of tumor sections to detect apoptosis in vivo . (I) Western blot analysis of PARP, p-Bcl-2, Bax and C-caspase-9 protein expression in tumor sections. (J) In the serum of each group of tumor-bearing mice, the results of blood biochemistry-related indexes were analyzed.

Journal: Bioactive Materials

Article Title: Translational selenium nanoparticles trigger apoptosis in triple-negative breast cancer cells through the MAPKs/Bcl2 pathway

doi: 10.1016/j.bioactmat.2026.02.027

Figure Lengend Snippet: In vivo anti-tumor efficacy of MUC1@PTR- SeNPs. (A) MUC1 mRNA expression in normal tissue and primary breast cancer tumor using GEPIA database. ( B ) MUC1 expression in tumor tissues of MDA-MB-468-bearing mice in preliminary study. (C – E) Dose-dependent study of tumor inhibition effect of MUC1@PTR-SeNPs [75 (Low), 375 (Mid) & 750 μg (High) Se/kg BW/day] on BALB/c nude mice transplanted with MDA-MB-468 xenograft after oral administration for 30 days. PTR-SeNPs (High; 750 μg Se/kg BW/day) was used to investigate the possible improvement of in vivo anti-tumor efficacy by the MUC1@PTR-SeNPs. Quantitative analysis of Se content (μg/g) in (F) blood and (G) tumor tissue of experimental mice. (H) H&E, Ki67 and Tunnel fluorescence staining of tumor sections to detect apoptosis in vivo . (I) Western blot analysis of PARP, p-Bcl-2, Bax and C-caspase-9 protein expression in tumor sections. (J) In the serum of each group of tumor-bearing mice, the results of blood biochemistry-related indexes were analyzed.

Article Snippet: Anti-human MUC1 therapeutic antibody Fab fragment (7B8) were purchased From Creative Biolabs (TAB-423MZ-F, USA).

Techniques: In Vivo, Expressing, Inhibition, Fluorescence, Staining, Western Blot

Cardiac IL-12β expression was significantly increased after TAC. (A) Western blots and quantified data of LV IL-12β expression in WT sham and WT TAC mice. (B) Representative LV IL-12β staining images and quantified data of IL-12β + area. (C) Representative images of IL-12β and CD45 co-immunostaining of WT mice LV tissue under sham and TAC conditions. The green stain in panel B is due to cardiac autofluorescence recorded at FITC channel. ∗p < 0.05; n = 5 per group.

Journal: Redox Biology

Article Title: Genetic inhibition of IL-12β suppresses systolic overload-induced cardiac oxidative stress, inflammation, and heart failure development

doi: 10.1016/j.redox.2026.104082

Figure Lengend Snippet: Cardiac IL-12β expression was significantly increased after TAC. (A) Western blots and quantified data of LV IL-12β expression in WT sham and WT TAC mice. (B) Representative LV IL-12β staining images and quantified data of IL-12β + area. (C) Representative images of IL-12β and CD45 co-immunostaining of WT mice LV tissue under sham and TAC conditions. The green stain in panel B is due to cardiac autofluorescence recorded at FITC channel. ∗p < 0.05; n = 5 per group.

Article Snippet: Anti-IL-12β antibody treatment: Pharmacological inhibition of IL-12β was achieved by anti-IL-12β antibody treatment (BioXCell, BE0051) in WT female mice.

Techniques: Expressing, Western Blot, Staining, Immunostaining

IL-12β KO significantly attenuated TAC-induced cardiac dysfunction, an increase in LV weight, LA weight, lung weight, and RV weight in male and female mice. (A) Representative M-mode echocardiographic images of WT and IL-12β KO male mice: pre-TAC, 2 weeks, 4 weeks, and 6 weeks after TAC, and Quantified data of echocardiographic measurements of LVEF, LVFS, LVESD, and LVEDD of both sexes. (B) Survival curves of WT TAC and IL-12β KO TAC mice of both sexes (log-rank test). (C–F) The ratio of LV weight, left atrial (LA) weight, lung weight, RV weight to tibial length (TL) of the indicated groups. (G) Representative LV WGA staining images and quantified data of cardiomyocyte cross-sectional areas. ∗p < 0.05; # p < 0.05 compared to WT sham; † p < 0.05 compared to WT TAC; $ p < 0.05 compared to IL-12β KO sham; n = 7 to 22 per group for panels A-F and n = 4-5 per group for panel G; LVEF, LV ejection fraction; LVFS, LV fractional shortening; LVESD, LV end-systolic diameter; LVEDD, LV end-diastolic diameter.

Journal: Redox Biology

Article Title: Genetic inhibition of IL-12β suppresses systolic overload-induced cardiac oxidative stress, inflammation, and heart failure development

doi: 10.1016/j.redox.2026.104082

Figure Lengend Snippet: IL-12β KO significantly attenuated TAC-induced cardiac dysfunction, an increase in LV weight, LA weight, lung weight, and RV weight in male and female mice. (A) Representative M-mode echocardiographic images of WT and IL-12β KO male mice: pre-TAC, 2 weeks, 4 weeks, and 6 weeks after TAC, and Quantified data of echocardiographic measurements of LVEF, LVFS, LVESD, and LVEDD of both sexes. (B) Survival curves of WT TAC and IL-12β KO TAC mice of both sexes (log-rank test). (C–F) The ratio of LV weight, left atrial (LA) weight, lung weight, RV weight to tibial length (TL) of the indicated groups. (G) Representative LV WGA staining images and quantified data of cardiomyocyte cross-sectional areas. ∗p < 0.05; # p < 0.05 compared to WT sham; † p < 0.05 compared to WT TAC; $ p < 0.05 compared to IL-12β KO sham; n = 7 to 22 per group for panels A-F and n = 4-5 per group for panel G; LVEF, LV ejection fraction; LVFS, LV fractional shortening; LVESD, LV end-systolic diameter; LVEDD, LV end-diastolic diameter.

Article Snippet: Anti-IL-12β antibody treatment: Pharmacological inhibition of IL-12β was achieved by anti-IL-12β antibody treatment (BioXCell, BE0051) in WT female mice.

Techniques: Staining

IL-12β KO attenuated TAC-induced alterations in the gene expression related to fibrosis and inflammation (A) Principal component analysis of WT and IL-12β KO mice, under sham or TAC conditions. (B) Venn diagram showing differentially expressed genes (DEGs) of WT and IL-12β KO mice under sham or TAC conditions, as well as the shared and uniquely changed genes. (C) DEGs cluster heatmap in WT mice compared to IL-12β KO mice, under sham or TAC conditions. (D) Volcano plots showing upregulated and downregulated genes among the groups. (E) Gene ontology (GO) biological processes enrichment bubble chart in WT TAC mice compared to IL-12β KO TAC. (F) GO cellular components enrichment histogram shows the enriched cellular components between KO and WT mice after TAC. n = 2 per group for sham and n = 3 per group for TAC.

Journal: Redox Biology

Article Title: Genetic inhibition of IL-12β suppresses systolic overload-induced cardiac oxidative stress, inflammation, and heart failure development

doi: 10.1016/j.redox.2026.104082

Figure Lengend Snippet: IL-12β KO attenuated TAC-induced alterations in the gene expression related to fibrosis and inflammation (A) Principal component analysis of WT and IL-12β KO mice, under sham or TAC conditions. (B) Venn diagram showing differentially expressed genes (DEGs) of WT and IL-12β KO mice under sham or TAC conditions, as well as the shared and uniquely changed genes. (C) DEGs cluster heatmap in WT mice compared to IL-12β KO mice, under sham or TAC conditions. (D) Volcano plots showing upregulated and downregulated genes among the groups. (E) Gene ontology (GO) biological processes enrichment bubble chart in WT TAC mice compared to IL-12β KO TAC. (F) GO cellular components enrichment histogram shows the enriched cellular components between KO and WT mice after TAC. n = 2 per group for sham and n = 3 per group for TAC.

Article Snippet: Anti-IL-12β antibody treatment: Pharmacological inhibition of IL-12β was achieved by anti-IL-12β antibody treatment (BioXCell, BE0051) in WT female mice.

Techniques: Gene Expression

IL-12β KO suppressed LV genetic pathways associated with extracellular matrix remodeling, inflammation, and LV fibrosis in mice after TAC. (A) The top 20 upregulated and downregulated pathways between KO and WT mice after TAC, identified by GSEA with ReactomeGSA. (B) Representative GSEA plots of collagen formation and extracellular matrix organization. (C, D) Representative images and quantified data of LV interstitial and perivascular fibrosis performed by Sirius Red/Fast Green staining in male and female mice. # p < 0.05 compared to WT sham; † p < 0.05 compared to WT TAC; $ p < 0.05 compared to IL-12β KO sham; n = 3 per group for panels A-B and n = 4-5 per group for panel D.

Journal: Redox Biology

Article Title: Genetic inhibition of IL-12β suppresses systolic overload-induced cardiac oxidative stress, inflammation, and heart failure development

doi: 10.1016/j.redox.2026.104082

Figure Lengend Snippet: IL-12β KO suppressed LV genetic pathways associated with extracellular matrix remodeling, inflammation, and LV fibrosis in mice after TAC. (A) The top 20 upregulated and downregulated pathways between KO and WT mice after TAC, identified by GSEA with ReactomeGSA. (B) Representative GSEA plots of collagen formation and extracellular matrix organization. (C, D) Representative images and quantified data of LV interstitial and perivascular fibrosis performed by Sirius Red/Fast Green staining in male and female mice. # p < 0.05 compared to WT sham; † p < 0.05 compared to WT TAC; $ p < 0.05 compared to IL-12β KO sham; n = 3 per group for panels A-B and n = 4-5 per group for panel D.

Article Snippet: Anti-IL-12β antibody treatment: Pharmacological inhibition of IL-12β was achieved by anti-IL-12β antibody treatment (BioXCell, BE0051) in WT female mice.

Techniques: Staining

IL-12β KO significantly attenuated TAC-induced LV inflammation in mice. (A) The top 20 upregulated and downregulated pathways between KO and WT mice after TAC were identified by GSEA with KEGG pathway analysis. (B) Heatmap shows the top LV immune and/or inflammation-related genes in KO and WT mice after TAC. (C, D) Representative LV CD45 + immuno-staining images and quantified data of LV CD45 + of the indicated groups. (E) Percentage distribution of major immune cell subsets within LV CD45 + cells of the indicated groups determined by flow cytometry. The green stain in panel C is due to cardiac autofluorescence recorded at FITC channel. # p < 0.05 compared to WT sham; † p < 0.05 compared to WT TAC; $ p < 0.05 compared to IL-12β KO sham; n = 2-3 per group for panels A-B and n = 4-5 per group for panels D-E.

Journal: Redox Biology

Article Title: Genetic inhibition of IL-12β suppresses systolic overload-induced cardiac oxidative stress, inflammation, and heart failure development

doi: 10.1016/j.redox.2026.104082

Figure Lengend Snippet: IL-12β KO significantly attenuated TAC-induced LV inflammation in mice. (A) The top 20 upregulated and downregulated pathways between KO and WT mice after TAC were identified by GSEA with KEGG pathway analysis. (B) Heatmap shows the top LV immune and/or inflammation-related genes in KO and WT mice after TAC. (C, D) Representative LV CD45 + immuno-staining images and quantified data of LV CD45 + of the indicated groups. (E) Percentage distribution of major immune cell subsets within LV CD45 + cells of the indicated groups determined by flow cytometry. The green stain in panel C is due to cardiac autofluorescence recorded at FITC channel. # p < 0.05 compared to WT sham; † p < 0.05 compared to WT TAC; $ p < 0.05 compared to IL-12β KO sham; n = 2-3 per group for panels A-B and n = 4-5 per group for panels D-E.

Article Snippet: Anti-IL-12β antibody treatment: Pharmacological inhibition of IL-12β was achieved by anti-IL-12β antibody treatment (BioXCell, BE0051) in WT female mice.

Techniques: Immunostaining, Flow Cytometry, Staining

IL-12β KO attenuated TAC-induced pulmonary inflammation, fibrosis, and vessel remodeling in male and female mice. (A, B) Representative images and quantified data of infiltrated CD45 + leukocytes in the lung performed by immuno-histological staining. (C, D) Representative images and quantified data of lung fibrosis performed by Sirius Red/Fast Green staining. (E, F) Representative images and quantified data of lung vessel remodeling performed by immuno-histological staining. # p < 0.05 compared to WT sham; † p < 0.05 compared to WT TAC; $ p < 0.05 compared to IL-12β KO sham; n = 4-5 per group.

Journal: Redox Biology

Article Title: Genetic inhibition of IL-12β suppresses systolic overload-induced cardiac oxidative stress, inflammation, and heart failure development

doi: 10.1016/j.redox.2026.104082

Figure Lengend Snippet: IL-12β KO attenuated TAC-induced pulmonary inflammation, fibrosis, and vessel remodeling in male and female mice. (A, B) Representative images and quantified data of infiltrated CD45 + leukocytes in the lung performed by immuno-histological staining. (C, D) Representative images and quantified data of lung fibrosis performed by Sirius Red/Fast Green staining. (E, F) Representative images and quantified data of lung vessel remodeling performed by immuno-histological staining. # p < 0.05 compared to WT sham; † p < 0.05 compared to WT TAC; $ p < 0.05 compared to IL-12β KO sham; n = 4-5 per group.

Article Snippet: Anti-IL-12β antibody treatment: Pharmacological inhibition of IL-12β was achieved by anti-IL-12β antibody treatment (BioXCell, BE0051) in WT female mice.

Techniques: Staining

IL-12β KO significantly attenuated TAC-induced early-phase LV dysfunction, cardiomyocyte hypertrophy, and inflammation. (A) Representative M-mode echocardiographic images and quantified data of echocardiographic measurements of LVEF, LVFS, LVESD, and LVEDD of the indicated groups. (B) The ratios of cardiac and pulmonary tissues to tibial length (TL) of the indicated groups. (C, D) Representative images and quantified data of LV cardiomyocyte size and LV CD45 + cells of the indicated groups. (E) Percentage of major immune cell subsets within LV CD45 + cells determined by flow cytometry. (F) Representative flow cytometry plots and quantified data of CD44 + CD3 + , CD44 + CD4 + , and CD44 + CD8 + T cells within the corresponding T cells. The green stain in panel D is due to cardiac autofluorescence recorded at FITC channel. ∗p < 0.05; n = 5-10 per group.

Journal: Redox Biology

Article Title: Genetic inhibition of IL-12β suppresses systolic overload-induced cardiac oxidative stress, inflammation, and heart failure development

doi: 10.1016/j.redox.2026.104082

Figure Lengend Snippet: IL-12β KO significantly attenuated TAC-induced early-phase LV dysfunction, cardiomyocyte hypertrophy, and inflammation. (A) Representative M-mode echocardiographic images and quantified data of echocardiographic measurements of LVEF, LVFS, LVESD, and LVEDD of the indicated groups. (B) The ratios of cardiac and pulmonary tissues to tibial length (TL) of the indicated groups. (C, D) Representative images and quantified data of LV cardiomyocyte size and LV CD45 + cells of the indicated groups. (E) Percentage of major immune cell subsets within LV CD45 + cells determined by flow cytometry. (F) Representative flow cytometry plots and quantified data of CD44 + CD3 + , CD44 + CD4 + , and CD44 + CD8 + T cells within the corresponding T cells. The green stain in panel D is due to cardiac autofluorescence recorded at FITC channel. ∗p < 0.05; n = 5-10 per group.

Article Snippet: Anti-IL-12β antibody treatment: Pharmacological inhibition of IL-12β was achieved by anti-IL-12β antibody treatment (BioXCell, BE0051) in WT female mice.

Techniques: Flow Cytometry, Staining

IL-12β KO significantly attenuated

Journal: Redox Biology

Article Title: Genetic inhibition of IL-12β suppresses systolic overload-induced cardiac oxidative stress, inflammation, and heart failure development

doi: 10.1016/j.redox.2026.104082

Figure Lengend Snippet: IL-12β KO significantly attenuated "stem cell-like" central memory T cell activation and their IFNγ production in the drainage lymph nodes. (A, B) Percentages of major immune cell subsets within CD45 + cells in the drainage lymph nodes determined by flow cytometry. (C) Percentages of IFNγ + CD8 + and TNFα + CD8 + within CD8 + T cells. (D, E) Percentages of CXCR3 + CD4 + and CXCR3 + CD8 + T cells within CD4 + and CD8 + T cells, respectively. (F) Percentage of effective memory (CD44 + CD62L − ), naïve (CD44 − CD62L + ), and central memory (CD44 + CD62L + ) T cells of CD8 + T cells. ∗p < 0.05; T EM , Effective Memory T Cells; T naïve , Naïve T Cells; T CM , Central Memory T Cells; n = 4-5 per group.

Article Snippet: Anti-IL-12β antibody treatment: Pharmacological inhibition of IL-12β was achieved by anti-IL-12β antibody treatment (BioXCell, BE0051) in WT female mice.

Techniques: Activation Assay, Flow Cytometry

IL-12β KO and anti-IL-12β antibody treatment significantly attenuated TAC-induced LV oxidative stress. (A) Representative dihydroethidium (DHE) staining images and quantified data of DHE intensity of the indicated groups. (B) Representative western blots and quantification of LV 3-nitrotyrosine (3-NT) and 4-hydroxynonenal (4-HNE) of the indicated groups. (C-E) Representative DHE, 3-NT, and 4-HNE staining images, and quantified data of relative DHE, 3-NT, and 4-HNE intensity of the indicated groups. ∗p < 0.05; n = 5 to 6 per group.

Journal: Redox Biology

Article Title: Genetic inhibition of IL-12β suppresses systolic overload-induced cardiac oxidative stress, inflammation, and heart failure development

doi: 10.1016/j.redox.2026.104082

Figure Lengend Snippet: IL-12β KO and anti-IL-12β antibody treatment significantly attenuated TAC-induced LV oxidative stress. (A) Representative dihydroethidium (DHE) staining images and quantified data of DHE intensity of the indicated groups. (B) Representative western blots and quantification of LV 3-nitrotyrosine (3-NT) and 4-hydroxynonenal (4-HNE) of the indicated groups. (C-E) Representative DHE, 3-NT, and 4-HNE staining images, and quantified data of relative DHE, 3-NT, and 4-HNE intensity of the indicated groups. ∗p < 0.05; n = 5 to 6 per group.

Article Snippet: Anti-IL-12β antibody treatment: Pharmacological inhibition of IL-12β was achieved by anti-IL-12β antibody treatment (BioXCell, BE0051) in WT female mice.

Techniques: Staining, Western Blot