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pd 1  (Miltenyi Biotec)


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    Structured Review

    Miltenyi Biotec pd 1
    Pd 1, supplied by Miltenyi Biotec, used in various techniques. Bioz Stars score: 93/100, based on 68 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/pd+1/CD279+(PD1)+Antibody%2C+anti-human%2C+REAfinity/pm42455847-67-88-90
    Average 93 stars, based on 68 article reviews
    pd 1 - by Bioz Stars, 2026-10
    93/100 stars

    Images

    Related Articles

    Activation Assay:

    Article Title: Highly sensitive live-cell imaging-based cytotoxicity assay enables functional validation of rare epitope-specific CTLs
    Article Snippet: For frequency analysis of epitope-specific T cells, antibodies against CD3 (300448, BioLegend), CD4 (300528, BioLegend), and CD8 (562429, BD, Franklin Lakes, New Jersey, USA) and fixable live/dead NIR dye ( L34975 , ThermoFisher) were used. .. For activation/exhaustion marker analysis after the cytotoxicity assay, antibodies against CD8 (563256, BD), PD-1 (130-120-385, Miltenyi), and LAG3 (130-118-677, Miltenyi) and fixable live/dead green dye ( L34969 , ThermoFisher) were used. ..

    Marker:

    Article Title: Highly sensitive live-cell imaging-based cytotoxicity assay enables functional validation of rare epitope-specific CTLs
    Article Snippet: For frequency analysis of epitope-specific T cells, antibodies against CD3 (300448, BioLegend), CD4 (300528, BioLegend), and CD8 (562429, BD, Franklin Lakes, New Jersey, USA) and fixable live/dead NIR dye ( L34975 , ThermoFisher) were used. .. For activation/exhaustion marker analysis after the cytotoxicity assay, antibodies against CD8 (563256, BD), PD-1 (130-120-385, Miltenyi), and LAG3 (130-118-677, Miltenyi) and fixable live/dead green dye ( L34969 , ThermoFisher) were used. ..

    Cytotoxicity Assay:

    Article Title: Highly sensitive live-cell imaging-based cytotoxicity assay enables functional validation of rare epitope-specific CTLs
    Article Snippet: For frequency analysis of epitope-specific T cells, antibodies against CD3 (300448, BioLegend), CD4 (300528, BioLegend), and CD8 (562429, BD, Franklin Lakes, New Jersey, USA) and fixable live/dead NIR dye ( L34975 , ThermoFisher) were used. .. For activation/exhaustion marker analysis after the cytotoxicity assay, antibodies against CD8 (563256, BD), PD-1 (130-120-385, Miltenyi), and LAG3 (130-118-677, Miltenyi) and fixable live/dead green dye ( L34969 , ThermoFisher) were used. ..

    Blocking Assay:

    Article Title: Aurantio-obtusin modulates Wilms Tumour 1 within the breast tumour microenvironment reducing immunosuppression and tumour growth
    Article Snippet: .. PDOs were fixed in 100 μl of 4% paraformaldehyde for 30 min at room temperature, permeabilised with 100 μl of blocking buffer (0.5% Triton-X-100 and 1% BSA in DPBS) for 1 h at room temperature, and incubated with EpCAM-FITC (Miltenyi Biotec, 130–113–825; 1:50), CD3-APC (Miltenyi Biotec, 130–113–135; 1:50), GZMB-FITC (BioLegenf, 372,206; 1:10) and PD-1 (Miltenyi Biotec, 130–120–382; 1:50) antibodies in blocking buffer at 4°C overnight. ..

    Article Title: Aurantio-obtusin modulates Wilms Tumour 1 within the breast tumour microenvironment reducing immunosuppression and tumour growth.
    Article Snippet: .. PDOs were fixed in 100 μl of 4% paraformaldehyde for 30 min at room temperature, permeabilised with 100 μl of blocking buffer (0.5% Triton-X-100 and 1% BSA in DPBS) for 1 h at room temperature, and incubated with EpCAM-FITC (Miltenyi Biotec, 130–113–825; 1:50), CD3-APC (Miltenyi Biotec, 130–113–135; 1:50), GZMB-FITC (BioLegenf, 372,206; 1:10) and PD-1 (Miltenyi Biotec, 130–120–382; 1:50) antibodies in blocking buffer at 4°C overnight. ..

    Incubation:

    Article Title: Aurantio-obtusin modulates Wilms Tumour 1 within the breast tumour microenvironment reducing immunosuppression and tumour growth
    Article Snippet: .. PDOs were fixed in 100 μl of 4% paraformaldehyde for 30 min at room temperature, permeabilised with 100 μl of blocking buffer (0.5% Triton-X-100 and 1% BSA in DPBS) for 1 h at room temperature, and incubated with EpCAM-FITC (Miltenyi Biotec, 130–113–825; 1:50), CD3-APC (Miltenyi Biotec, 130–113–135; 1:50), GZMB-FITC (BioLegenf, 372,206; 1:10) and PD-1 (Miltenyi Biotec, 130–120–382; 1:50) antibodies in blocking buffer at 4°C overnight. ..

    Article Title: Aurantio-obtusin modulates Wilms Tumour 1 within the breast tumour microenvironment reducing immunosuppression and tumour growth.
    Article Snippet: .. PDOs were fixed in 100 μl of 4% paraformaldehyde for 30 min at room temperature, permeabilised with 100 μl of blocking buffer (0.5% Triton-X-100 and 1% BSA in DPBS) for 1 h at room temperature, and incubated with EpCAM-FITC (Miltenyi Biotec, 130–113–825; 1:50), CD3-APC (Miltenyi Biotec, 130–113–135; 1:50), GZMB-FITC (BioLegenf, 372,206; 1:10) and PD-1 (Miltenyi Biotec, 130–120–382; 1:50) antibodies in blocking buffer at 4°C overnight. ..

    Staining:

    Article Title: A novel Vδ1 engager targeting CD19 enhances human Vδ1 γδ T cell responses against CLL and CD19+ hematological malignancies.
    Article Snippet: γδ T cells are associated with favorable outcomes in many cancers likely through a mechanism of stress-directed cytotoxicity and antitumor cytokine production.. Vδ1 γδ T cells are especially promising for immunotherapy due to their broad stress recognition and resistance to activation-induced cell death.. Here, we generate a CD19 engager incorporating a novel Vδ1 binding moiety as proof-of-concept for treating CD19 cancers, including Chronic Lymphocytic Leukemia (CLL).

    Article Title: Autocrine signaling in hormonally active cancer induces antigen expression for immunotherapy
    Article Snippet: .. The following antibodies were used for cell staining: ROR1 (AF647, clone 2A2, BioLegend), CD45 (VioBlue, clone REA747, Miltenyi), CD4 (PeVio770, clone REA, Miltenyi), CD8 (APC-Cy7, clone SK1, BioLegend), tEGFR (APC, clone AY13, Bio-Legend), PD-1 (PE, clone PD1.3.1., Miltenyi), Lag3 (PerCP-Cy5.5, clone 11C3C65, Bio-Legend), CTLA-4 (PeCy7, clone L3D10, BioLegend), Tim-3 (CD366), APC-Cy7, clone F382E2, BioLegend), CD45RO (FITC, clone UCHL1, BioLegend), CD45RA (PE, clone T6D11, Miltenyi), CD62L (PerCP-Cy5.5, clone DREG-56, BioLegend), CD25, PeCy7, clone BC96, BioLegend), CD69 (APC-Cy7, clone FN50, BioLegend). .. Quantitative flow cytometry was performed using PE-labeled antibodies and the BD-Quantibrite PE-Bead Assay (BD Biosciences).

    Flow Cytometry:

    Article Title: A novel Vδ1 engager targeting CD19 enhances human Vδ1 γδ T cell responses against CLL and CD19+ hematological malignancies.
    Article Snippet: γδ T cells are associated with favorable outcomes in many cancers likely through a mechanism of stress-directed cytotoxicity and antitumor cytokine production.. Vδ1 γδ T cells are especially promising for immunotherapy due to their broad stress recognition and resistance to activation-induced cell death.. Here, we generate a CD19 engager incorporating a novel Vδ1 binding moiety as proof-of-concept for treating CD19 cancers, including Chronic Lymphocytic Leukemia (CLL).

    Imaging:

    Article Title: Inhibition of autophagy enhances the antitumor efficacy of T/CAR T cell against neuroblastoma
    Article Snippet: Fluorochromes were photobleached or released using REAlease technology (Miltenyi) after image acquisition at the end of each staining cycle. .. The following antibodies (all from Miltenyi Biotec) were used: Ki67, CD3, CD4, CD8, CD44, CD45RA, CD45RO, CD57, CD183, CD196, LAG3 (CD223), PD-1 (CD279), TIM3 (CD366), FoxP3, HLA-DR. Acquired images were processed and analyzed by MACSiQ ® View Imaging Software (Miltenyi Biotec) following current processing work-flow (Miltenyi Biotec). ..

    Software:

    Article Title: Inhibition of autophagy enhances the antitumor efficacy of T/CAR T cell against neuroblastoma
    Article Snippet: Fluorochromes were photobleached or released using REAlease technology (Miltenyi) after image acquisition at the end of each staining cycle. .. The following antibodies (all from Miltenyi Biotec) were used: Ki67, CD3, CD4, CD8, CD44, CD45RA, CD45RO, CD57, CD183, CD196, LAG3 (CD223), PD-1 (CD279), TIM3 (CD366), FoxP3, HLA-DR. Acquired images were processed and analyzed by MACSiQ ® View Imaging Software (Miltenyi Biotec) following current processing work-flow (Miltenyi Biotec). ..

    Bioprocessing:

    Article Title: Enhanced solid tumor cell targeting by a neoepitope-encoding oncolytic measles virus combined with CAR therapy
    Article Snippet: For evaluation of CAR-T cell activation, staining with CD137 (CD137 Antibody, PE-Vio770, anti-human, REAfinity) (Miltenyi Biotech, Bergisch Gladbach, Germany) was carried out after 24 h of co-incubation. .. For evaluation of CAR-T cell exhaustion, the monoclonal antibodies LAG-3 (CD223 Antibody, PE-Vio770, anti-human, REAfinity), PD-1 (CD279 Antibody, APC, anti-human, REAfinity), and TIM-3 (CD366 Antibody, PE-Vio615, anti-human, REAfinity) (all Miltenyi Biotec, Bergisch Gladbach, Germany) were used. ..

    Expressing:

    Article Title: Divergent on-target off-tumor effects by CAR T and CAR NK cells suggest different efficacy and safety of cell therapies
    Article Snippet: .. The mAbs LAG-3 (CD223 Antibody, anti-human, REAfinityTM, Cat# 130–127–931, RRID:AB_2904843), PD-1 (CD279 Antibody, anti-human, REAfinityTM, Cat# 130–120–389, RRID:AB_2752075) and SLAMF7 (CD319 (CRACC) Antibody, anti-human, REAfinityTM, Cat# 130–126–031, RRID:AB_2889550) (all purchased from Miltenyi Biotec, Bergisch Gladbach, Germany) were used for receptor expression on CAR cells on days 3, 6 and 10 post-transduction. .. Briefly, cells were incubated with the respective antibodies for 10 minutes at 4°C, washed once, and analyzed using a MacsQuant10 analyzer (Miltenyi Biotec, Bergisch Gladbach, Germany).



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    PD-1 H regulates GAM polarization to promote glioma malignancy and suppress T-cell immunity. ( A ) Flow cytometric analysis of CD206 expression in BV2 cells, used as an in vitro model of GAMs, with PD-1 H knockout (PD-1 H-KO and PD-1 H-KO#1) or negative control (PD-1 H-NC) under basal conditions (blank) or following IL-4 stimulation (M2) for 48 h. ( B ) Flow cytometric analysis of CD86 expression in PD-1 H-deficient or control BV2 cells under basal conditions (blank) or after IFN-γ stimulation (M1) for 48 h. ( C ) Phagocytic activity of PD-1 H-deficient and control BV2 cells, assessed by uptake of fluorescent microspheres (FluoSpheres) after 4 h incubation. ( D ) Cell viability of GL261 glioma cells cultured with conditioned media derived from PD-1 H-NC, PD-1 H-KO, PD-1 H-KO#1, lenti-NC, or PD-1 H-overexpressing BV2 cells, measured by CCK-8 assay at 24, 48, and 72 h (*** p < 0.001, **** p < 0.0001). ( E, F ) Transwell invasion assays of GL261 cells co-cultured with BV2 cells expressing different levels of PD-1 H. Representative images ( E ) and quantification of invading cells per field ( F ) Are shown (* p < 0.05). ( G, H ) Colony formation assay of GL261 cells cultured with conditioned medium from BV2 cells as indicated. Representative images ( G ) and quantification of colony numbers ( H ) are shown (* p < 0.05, ** p < 0.01). ( I, J ) Wound-healing assays of GL261 cells at 0 h and 48 h after scratch following treatment with BV2 cell–derived conditioned media. Representative images ( I ) and quantification of wound closure ( J ) Are shown (* p < 0.05, ** p < 0.01). ( K ) Antigen-specific proliferation of OT-I CD8+ T cells in the priming stage. Total lymph node cells were stimulated with OVA257-268 peptide and co-cultured with BV2 cells for 48 h. Representative CFSE histograms are shown. ( L ) Proliferation analysis of CD8+ T cells in the differentiation stage. Pre-primed T cells were co-cultured with BV2 cells under IL-2 stimulation for another 48 h. Relative proliferative capacity was quantified via derivative analysis of normalized CFSE signals. Data are presented as mean ± SD (** p < 0.01)
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    Image Search Results


    Representative PD-L1 immunohistochemical images showing high expression (CPS=80). The brown DAB staining indicates PD-L1 expression on the cell membrane, while blue hematoxylin counterstain marks the nuclei (magnification, ×200; scale bar, 100 µm).

    Journal: Oncology Letters

    Article Title: Long survival of PD-L1-positive mediastinal sarcomatoid carcinoma after immunotherapy and anti-angiogenic target therapy: A case report

    doi: 10.3892/ol.2026.15690

    Figure Lengend Snippet: Representative PD-L1 immunohistochemical images showing high expression (CPS=80). The brown DAB staining indicates PD-L1 expression on the cell membrane, while blue hematoxylin counterstain marks the nuclei (magnification, ×200; scale bar, 100 µm).

    Article Snippet: The specimen obtained via bronchoscopy was sent to Amoy Diagnostics Co., Ltd. for genomic and programmed cell death ligand 1 (PD-L1) testing; no pathogenic gene mutations were detected.

    Techniques: Immunohistochemical staining, Expressing, Staining, Membrane

    PD-1 H regulates GAM polarization to promote glioma malignancy and suppress T-cell immunity. ( A ) Flow cytometric analysis of CD206 expression in BV2 cells, used as an in vitro model of GAMs, with PD-1 H knockout (PD-1 H-KO and PD-1 H-KO#1) or negative control (PD-1 H-NC) under basal conditions (blank) or following IL-4 stimulation (M2) for 48 h. ( B ) Flow cytometric analysis of CD86 expression in PD-1 H-deficient or control BV2 cells under basal conditions (blank) or after IFN-γ stimulation (M1) for 48 h. ( C ) Phagocytic activity of PD-1 H-deficient and control BV2 cells, assessed by uptake of fluorescent microspheres (FluoSpheres) after 4 h incubation. ( D ) Cell viability of GL261 glioma cells cultured with conditioned media derived from PD-1 H-NC, PD-1 H-KO, PD-1 H-KO#1, lenti-NC, or PD-1 H-overexpressing BV2 cells, measured by CCK-8 assay at 24, 48, and 72 h (*** p < 0.001, **** p < 0.0001). ( E, F ) Transwell invasion assays of GL261 cells co-cultured with BV2 cells expressing different levels of PD-1 H. Representative images ( E ) and quantification of invading cells per field ( F ) Are shown (* p < 0.05). ( G, H ) Colony formation assay of GL261 cells cultured with conditioned medium from BV2 cells as indicated. Representative images ( G ) and quantification of colony numbers ( H ) are shown (* p < 0.05, ** p < 0.01). ( I, J ) Wound-healing assays of GL261 cells at 0 h and 48 h after scratch following treatment with BV2 cell–derived conditioned media. Representative images ( I ) and quantification of wound closure ( J ) Are shown (* p < 0.05, ** p < 0.01). ( K ) Antigen-specific proliferation of OT-I CD8+ T cells in the priming stage. Total lymph node cells were stimulated with OVA257-268 peptide and co-cultured with BV2 cells for 48 h. Representative CFSE histograms are shown. ( L ) Proliferation analysis of CD8+ T cells in the differentiation stage. Pre-primed T cells were co-cultured with BV2 cells under IL-2 stimulation for another 48 h. Relative proliferative capacity was quantified via derivative analysis of normalized CFSE signals. Data are presented as mean ± SD (** p < 0.01)

    Journal: Journal of Translational Medicine

    Article Title: PD-1 H (VISTA) drives immunosuppressive reprogramming of glioma-associated myeloid cells to promote glioma progression

    doi: 10.1186/s12967-026-08497-0

    Figure Lengend Snippet: PD-1 H regulates GAM polarization to promote glioma malignancy and suppress T-cell immunity. ( A ) Flow cytometric analysis of CD206 expression in BV2 cells, used as an in vitro model of GAMs, with PD-1 H knockout (PD-1 H-KO and PD-1 H-KO#1) or negative control (PD-1 H-NC) under basal conditions (blank) or following IL-4 stimulation (M2) for 48 h. ( B ) Flow cytometric analysis of CD86 expression in PD-1 H-deficient or control BV2 cells under basal conditions (blank) or after IFN-γ stimulation (M1) for 48 h. ( C ) Phagocytic activity of PD-1 H-deficient and control BV2 cells, assessed by uptake of fluorescent microspheres (FluoSpheres) after 4 h incubation. ( D ) Cell viability of GL261 glioma cells cultured with conditioned media derived from PD-1 H-NC, PD-1 H-KO, PD-1 H-KO#1, lenti-NC, or PD-1 H-overexpressing BV2 cells, measured by CCK-8 assay at 24, 48, and 72 h (*** p < 0.001, **** p < 0.0001). ( E, F ) Transwell invasion assays of GL261 cells co-cultured with BV2 cells expressing different levels of PD-1 H. Representative images ( E ) and quantification of invading cells per field ( F ) Are shown (* p < 0.05). ( G, H ) Colony formation assay of GL261 cells cultured with conditioned medium from BV2 cells as indicated. Representative images ( G ) and quantification of colony numbers ( H ) are shown (* p < 0.05, ** p < 0.01). ( I, J ) Wound-healing assays of GL261 cells at 0 h and 48 h after scratch following treatment with BV2 cell–derived conditioned media. Representative images ( I ) and quantification of wound closure ( J ) Are shown (* p < 0.05, ** p < 0.01). ( K ) Antigen-specific proliferation of OT-I CD8+ T cells in the priming stage. Total lymph node cells were stimulated with OVA257-268 peptide and co-cultured with BV2 cells for 48 h. Representative CFSE histograms are shown. ( L ) Proliferation analysis of CD8+ T cells in the differentiation stage. Pre-primed T cells were co-cultured with BV2 cells under IL-2 stimulation for another 48 h. Relative proliferative capacity was quantified via derivative analysis of normalized CFSE signals. Data are presented as mean ± SD (** p < 0.01)

    Article Snippet: Mice were subsequently treated with PBS or anti-PD-1 H monoclonal antibody (13F3, 300 μg/mouse, HY-P990145, MCE) every two days, a dosing regimen based on previous studies [ , ].

    Techniques: Expressing, In Vitro, Knock-Out, Negative Control, Control, Activity Assay, Incubation, Cell Culture, Derivative Assay, CCK-8 Assay, Colony Assay

    PD-1 H expression and distribution in glioma. ( A ) Representative IHC images of PD-1 H in human glioma vs. normal brain tissue (scale bars, 200 μm). ( B ) Quantification of IHC scores for PD-1 H in glioma ( n = 27) and normal brain ( n = 5) samples (** p < 0.01). ( C ) Violin plots showing expression distribution of PD-1 H and other immune checkpoint molecules (TIM-3, LAG-3, TIGIT, CTLA-4, PD-L1, and PD-1) in glioma samples from the TCGA dataset. ( D ) Bulk RNA-seq of PD-1 H expression levels in glioma ( n = 702) and normal brain ( n = 423) samples based on RNA-seq data from TCGA and GTEx datasets (**** p < 0.0001). ( E ) UMAP plot showing single-cell RNA-seq data of glioma, colored by cell type (5.27 × 10 5 cells from 85 glioma samples, single-cell portal, SCP2389). ( F ) UMAP plot with PD-1 H expression intensity (color scale). ( G ) Bar chart showing the expression of PD-1 H in different cell clusters

    Journal: Journal of Translational Medicine

    Article Title: PD-1 H (VISTA) drives immunosuppressive reprogramming of glioma-associated myeloid cells to promote glioma progression

    doi: 10.1186/s12967-026-08497-0

    Figure Lengend Snippet: PD-1 H expression and distribution in glioma. ( A ) Representative IHC images of PD-1 H in human glioma vs. normal brain tissue (scale bars, 200 μm). ( B ) Quantification of IHC scores for PD-1 H in glioma ( n = 27) and normal brain ( n = 5) samples (** p < 0.01). ( C ) Violin plots showing expression distribution of PD-1 H and other immune checkpoint molecules (TIM-3, LAG-3, TIGIT, CTLA-4, PD-L1, and PD-1) in glioma samples from the TCGA dataset. ( D ) Bulk RNA-seq of PD-1 H expression levels in glioma ( n = 702) and normal brain ( n = 423) samples based on RNA-seq data from TCGA and GTEx datasets (**** p < 0.0001). ( E ) UMAP plot showing single-cell RNA-seq data of glioma, colored by cell type (5.27 × 10 5 cells from 85 glioma samples, single-cell portal, SCP2389). ( F ) UMAP plot with PD-1 H expression intensity (color scale). ( G ) Bar chart showing the expression of PD-1 H in different cell clusters

    Article Snippet: Mice were subsequently treated with PBS or anti-PD-1 H monoclonal antibody (13F3, 300 μg/mouse, HY-P990145, MCE) every two days, a dosing regimen based on previous studies [ , ].

    Techniques: Expressing, RNA Sequencing, Single Cell

    PD-1 H expression in GAMs is associated with immune cell composition and clinical outcome in glioma. ( A–E ) Representative IHC staining of PD-1 H, CD68, CD163, CD80, and CD8 in a glioma specimen with low PD-1 H expression (patient-1). ( F–J ) Corresponding IHC staining of PD-1 H, CD68, CD163, CD80, and CD8 in a glioma specimen with high PD-1 H expression (patient-2). Scale bars, 200 μm. ( K–N ) Correlation analyses between PD-1 H and immune cell markers, including CD68, CD163, CD80 and CD8 in glioma samples ( n = 27). ( O–R ) Correlation analyses of expression levels between PD-1 H and immune checkpoint molecules, including TIM-3, PD-L1, PD-1, and CTLA-4 in glioma samples from the TCGA dataset ( n = 702, Spearman correlation, p < 0.001). ( S, T ) Kaplan–Meier survival curves of glioma patients stratified by PD-1 H expression levels in GAMs, including progression-free survival (PFS, S) and overall survival (OS, T) (Log-rank test)

    Journal: Journal of Translational Medicine

    Article Title: PD-1 H (VISTA) drives immunosuppressive reprogramming of glioma-associated myeloid cells to promote glioma progression

    doi: 10.1186/s12967-026-08497-0

    Figure Lengend Snippet: PD-1 H expression in GAMs is associated with immune cell composition and clinical outcome in glioma. ( A–E ) Representative IHC staining of PD-1 H, CD68, CD163, CD80, and CD8 in a glioma specimen with low PD-1 H expression (patient-1). ( F–J ) Corresponding IHC staining of PD-1 H, CD68, CD163, CD80, and CD8 in a glioma specimen with high PD-1 H expression (patient-2). Scale bars, 200 μm. ( K–N ) Correlation analyses between PD-1 H and immune cell markers, including CD68, CD163, CD80 and CD8 in glioma samples ( n = 27). ( O–R ) Correlation analyses of expression levels between PD-1 H and immune checkpoint molecules, including TIM-3, PD-L1, PD-1, and CTLA-4 in glioma samples from the TCGA dataset ( n = 702, Spearman correlation, p < 0.001). ( S, T ) Kaplan–Meier survival curves of glioma patients stratified by PD-1 H expression levels in GAMs, including progression-free survival (PFS, S) and overall survival (OS, T) (Log-rank test)

    Article Snippet: Mice were subsequently treated with PBS or anti-PD-1 H monoclonal antibody (13F3, 300 μg/mouse, HY-P990145, MCE) every two days, a dosing regimen based on previous studies [ , ].

    Techniques: Expressing, Immunohistochemistry

    PD-1 H expression in GAMs promotes glioma progression and impairs antitumor T-cell responses in vivo. ( A ) Schematic illustration of the in vivo experimental design. C57BL/6 mice were intracranially implanted with GL261-luc glioma cells together with GAMs expressing PD-1 H overexpression (PD-1 H-OE), negative control (PD-1 H-NC), or PD-1 H knockout (PD-1 H-KO). Tumor growth was monitored by bioluminescence imaging at the indicated time points. ( B ) Representative bioluminescence images of tumor-bearing mice from each group at days 7, 14, and 21 after implantation. ( C ) Quantification of tumor bioluminescence radiance over time in mice receiving PD-1 H-OE, PD-1 H-NC, or PD-1 H-KO GAMs (* p < 0.05, *** p < 0.001). ( D ) Kaplan–Meier survival analysis of glioma-bearing mice in the indicated groups. Statistical significance was determined by log-rank test ( p < 0.001). ( E ) Flow cytometric analysis of GAM phenotypes isolated from glioma tissues. Representative histograms show expression of CD206 and MHC-II on GAMs from PD-1 H-OE, PD-1 H-NC, and PD-1 H-KO groups. ( F, G ) Representative flow cytometry histograms showing expression of PD-1 and TIM-3 on tumor-infiltrating CD8 + T ( F ) and CD4 + T ( G ) cells from each group

    Journal: Journal of Translational Medicine

    Article Title: PD-1 H (VISTA) drives immunosuppressive reprogramming of glioma-associated myeloid cells to promote glioma progression

    doi: 10.1186/s12967-026-08497-0

    Figure Lengend Snippet: PD-1 H expression in GAMs promotes glioma progression and impairs antitumor T-cell responses in vivo. ( A ) Schematic illustration of the in vivo experimental design. C57BL/6 mice were intracranially implanted with GL261-luc glioma cells together with GAMs expressing PD-1 H overexpression (PD-1 H-OE), negative control (PD-1 H-NC), or PD-1 H knockout (PD-1 H-KO). Tumor growth was monitored by bioluminescence imaging at the indicated time points. ( B ) Representative bioluminescence images of tumor-bearing mice from each group at days 7, 14, and 21 after implantation. ( C ) Quantification of tumor bioluminescence radiance over time in mice receiving PD-1 H-OE, PD-1 H-NC, or PD-1 H-KO GAMs (* p < 0.05, *** p < 0.001). ( D ) Kaplan–Meier survival analysis of glioma-bearing mice in the indicated groups. Statistical significance was determined by log-rank test ( p < 0.001). ( E ) Flow cytometric analysis of GAM phenotypes isolated from glioma tissues. Representative histograms show expression of CD206 and MHC-II on GAMs from PD-1 H-OE, PD-1 H-NC, and PD-1 H-KO groups. ( F, G ) Representative flow cytometry histograms showing expression of PD-1 and TIM-3 on tumor-infiltrating CD8 + T ( F ) and CD4 + T ( G ) cells from each group

    Article Snippet: Mice were subsequently treated with PBS or anti-PD-1 H monoclonal antibody (13F3, 300 μg/mouse, HY-P990145, MCE) every two days, a dosing regimen based on previous studies [ , ].

    Techniques: Expressing, In Vivo, Over Expression, Negative Control, Knock-Out, Imaging, Isolation, Flow Cytometry

    PD-1 H regulates transcriptional programs and signaling pathways in GAMs. ( A ) Principal component analysis (PCA) of transcriptomic profiles from BV2 cells with PD-1 H-KO (KO), PD-1 H-NC (NC), or PD-1 H-OE (OE), showing distinct clustering among groups. ( B, C ) Volcano plot ( B ) and heatmap ( C ) showing differentially expressed genes (DEGs) in PD-1 H-OE vs. PD-1 H-NC. Upregulated and downregulated genes are highlighted. ( D, E ) Volcano plot ( D ) and heatmap ( E ) displaying DEGs in PD-1 H-KO vs. PD-1 H-NC. ( F, G ) Gene ontology (GO) enrichment analysis of DEGs from PD-1 H-OE vs. PD-1 H-NC ( F ) and PD-1 H-KO vs. PD-1 H-NC ( G ), with dot size indicating gene count and color representing statistical significance. ( H ) Western blot analysis of NF-κB, phosphorylated AKT (p-AKT), total AKT, in BV2 cells with different expression levels of PD-1 H. The PD-1H-blocking antibody 13F3 was applied as indicated (−/+)

    Journal: Journal of Translational Medicine

    Article Title: PD-1 H (VISTA) drives immunosuppressive reprogramming of glioma-associated myeloid cells to promote glioma progression

    doi: 10.1186/s12967-026-08497-0

    Figure Lengend Snippet: PD-1 H regulates transcriptional programs and signaling pathways in GAMs. ( A ) Principal component analysis (PCA) of transcriptomic profiles from BV2 cells with PD-1 H-KO (KO), PD-1 H-NC (NC), or PD-1 H-OE (OE), showing distinct clustering among groups. ( B, C ) Volcano plot ( B ) and heatmap ( C ) showing differentially expressed genes (DEGs) in PD-1 H-OE vs. PD-1 H-NC. Upregulated and downregulated genes are highlighted. ( D, E ) Volcano plot ( D ) and heatmap ( E ) displaying DEGs in PD-1 H-KO vs. PD-1 H-NC. ( F, G ) Gene ontology (GO) enrichment analysis of DEGs from PD-1 H-OE vs. PD-1 H-NC ( F ) and PD-1 H-KO vs. PD-1 H-NC ( G ), with dot size indicating gene count and color representing statistical significance. ( H ) Western blot analysis of NF-κB, phosphorylated AKT (p-AKT), total AKT, in BV2 cells with different expression levels of PD-1 H. The PD-1H-blocking antibody 13F3 was applied as indicated (−/+)

    Article Snippet: Mice were subsequently treated with PBS or anti-PD-1 H monoclonal antibody (13F3, 300 μg/mouse, HY-P990145, MCE) every two days, a dosing regimen based on previous studies [ , ].

    Techniques: Protein-Protein interactions, Western Blot, Expressing, Blocking Assay

    Therapeutic blockade of PD-1 H suppresses glioma progression in PD-1 H-/- host mice. ( A ) Schematic illustration of the in vivo experimental design. C57BL/6PD-1 H-/- mice were intracranially implanted with GL261-luc glioma cells together with PD-1 H-NC GAMs. Mice were treated with PBS or anti-PD-1 H monoclonal antibody at the indicated time points, and tumor growth was monitored by serial bioluminescence imaging. ( B ) Representative bioluminescence images of mice treated with PBS or anti-PD-1 H antibody at days 7, 14, 21, and 28 after implantation. ( C ) Quantification of tumor bioluminescence radiance over time in PBS- and anti-PD-1 H-treated mice, * p < 0.05. ( D ) Kaplan–Meier survival curves of glioma-bearing mice receiving PBS or anti-PD-1 H treatment, log-rank test, * p < 0.05

    Journal: Journal of Translational Medicine

    Article Title: PD-1 H (VISTA) drives immunosuppressive reprogramming of glioma-associated myeloid cells to promote glioma progression

    doi: 10.1186/s12967-026-08497-0

    Figure Lengend Snippet: Therapeutic blockade of PD-1 H suppresses glioma progression in PD-1 H-/- host mice. ( A ) Schematic illustration of the in vivo experimental design. C57BL/6PD-1 H-/- mice were intracranially implanted with GL261-luc glioma cells together with PD-1 H-NC GAMs. Mice were treated with PBS or anti-PD-1 H monoclonal antibody at the indicated time points, and tumor growth was monitored by serial bioluminescence imaging. ( B ) Representative bioluminescence images of mice treated with PBS or anti-PD-1 H antibody at days 7, 14, 21, and 28 after implantation. ( C ) Quantification of tumor bioluminescence radiance over time in PBS- and anti-PD-1 H-treated mice, * p < 0.05. ( D ) Kaplan–Meier survival curves of glioma-bearing mice receiving PBS or anti-PD-1 H treatment, log-rank test, * p < 0.05

    Article Snippet: Mice were subsequently treated with PBS or anti-PD-1 H monoclonal antibody (13F3, 300 μg/mouse, HY-P990145, MCE) every two days, a dosing regimen based on previous studies [ , ].

    Techniques: In Vivo, Imaging