cd70 antibody  (Cell Signaling Technology Inc)

Journal: bioRxiv

Article Title: Transient immune landscape remodelling shapes CD8 T-cell priming during infection

doi: 10.64898/2026.03.18.712682

Figure Lengend Snippet: (A-B) Graphs show XCR1 (A) and SIRPa (B) signal density within innate-infiltrated and non-infiltrated regions on stained spleen sections harvested 24hrs after LM-OVA infection (n=5). C- Mice were adoptively transferred with OTIxGFP T-cells and infected with LM-OVA. After 24hrs, spleen sections were stained for CD169 (red), 33D1 (magenta), XCR1 (cyan), OTI (green). Representative image. (D-F) Mice were infected with LM-OVA for 24hrs and splenocytes were analysed by flow cytometry. Graphs show CD80 MFI ( D , n=5-7), CD86 MFI ( E , n=5-7), and frequency of CD70+ cDC1 and cDC2 ( F , n=4-5). (G-H) Spleen sections from mice infected with LM-OVA for 24hrs were stained for CD169 (blue), CD70 (red), CD11b (white). G- Representative image. H- Graph shows CD70 signal intensity within innate-infiltrated and non-infiltrated regions in WPs (n=5). I-K Mice were infected with LM-OVA and treated with anti-CXCR3 or anti-CD70 antibodies as indicated 6hrs before infection. Graphs show frequencies (I) , absolute numbers (J) and avidity (K) of N4-tetramer+ CD8 T-cells 8 days post-infection (n=12-17 per group). Ratio paired t-tests (A-B, D-F, H) , Welch and Brown-Forsythe one-way ANOVA with Dunnett’s multiple comparisons test (I-K) .

Article Snippet: For CD70 blockade, mice were intraperitoneally administered 300μg anti-CD70 antibody (BioXCell, BE0022) or isotype control antibody (BioXcell, BE0290) 6hr before infection, either alone or in combination with CXCR3 blockade.

Techniques: Staining, Infection, Flow Cytometry

Journal: bioRxiv

Article Title: Transient immune landscape remodelling shapes CD8 T-cell priming during infection

doi: 10.64898/2026.03.18.712682

Figure Lengend Snippet: (A-B) Representative image of spleen sections from mice infected with LM-OVA for 24hrs were stained for CD169 (blue), XCR1 (cyan), NKp46 (red) and SIRPa ( A , magenta), or 33D1 ( B , magenta). C- Mice were adoptively transferred with OTIxGFP cells and infected with LM-OVA. Representative image of spleen sections stained for CD169 (red), 33D1 (magenta), XCR1 (cyan), OTI (green) 24hrs post-infection. (D-E) Splenocytes from mice infected with LM-OVA for 24hrs were analysed by flow cytometry. D- Representative gating strategy for splenic cDC1 and cDC2 subsets. E- Representative histograms showing CD80, CD86, and CD70 expression in cDC1 and cDC2.

Article Snippet: For CD70 blockade, mice were intraperitoneally administered 300μg anti-CD70 antibody (BioXCell, BE0022) or isotype control antibody (BioXcell, BE0290) 6hr before infection, either alone or in combination with CXCR3 blockade.

Techniques: Infection, Staining, Flow Cytometry, Expressing

Journal: Blood Cancer Discovery

Article Title: CD70-Targeting CAR NK Cells Overcome BCMA Downregulation and Improve Survival in High-risk Multiple Myeloma Models

doi: 10.1158/2643-3230.BCD-25-0130

Figure Lengend Snippet: CD70 expression in patients with multiple myeloma. Comparison of CD70 mRNA levels based on ( A ) RNA levels from the MMRF CoMMpass dataset of different translocations, Amp1q and Del17p, in patients with NDMM and ( B ) the ISS ( n = 561). C, Paired comparison of CD70 mRNA in NDMM and at first relapse (left). The difference between the expression levels is plotted (right, relapsed–NDMM) with a dotted line at the mean of differences (0.609, P = 0.0028, paired t test, n = 61). D, Patients were stratified into tertiles based on CD70 mRNA expression, and overall survival (OS) was plotted ( n = 792). Color shading represents the 95% confidence interval. E, Bone marrow aspirates from patients with multiple myeloma ( n = 46) from the MD Anderson Cancer Center with different translocations involving chromosome 14 were analyzed for CD70 mRNA using the pseudobulk approach on single cell (sc)-mRNA. The control group included samples from n = 3 healthy control donors. The fourth data point in the control group represents nontumor or polyclonal plasma cells (PC) from patients with multiple myeloma identified by the expression of B-cell receptor VDJ using scRNA-seq (see “Methods”); monoclonal plasma cells were similarly defined based on BCR VDJ sequences, and each remaining data point corresponds to an individual patient with multiple myeloma: no translocation (none; n = 20), t(11;14) ( n = 16), t(14;16) ( n = 2), and t(4;14) ( n = 8). F, The sc-mRNA transcriptome data from all samples projected onto a Uniform Manifold Approximation and Projection for Dimension Reduction (UMAP). Individual CD70 mRNA was mapped at single-cell resolution. G, Translocations involving the immunoglobulin heavy chain locus identified by FISH are mapped onto a UMAP. Box and whisker plots show the median and IQR (25th and 75th percentiles), and the whiskers extend to ±1.5 times the IQR. The P values were determined by the Wilcoxon test [ A , B , D (left panel) and E ]. *, P ≤ 0.05; **, P ≤ 0.01; ***, P ≤ 0.001; ns, not significant. UMI, unique molecular identifier.

Article Snippet: The CD70 antibody (Cell Signaling Technology, clone e3Q1A, cat. #69209S) was used at a 1:50 dilution, incubated for 15 minutes at room temperature, and subsequently detected using the BOND Polymer Refine Detection kit (Leica Biosystems, cat. #DS9800) with diaminobenzidine as the chromogen and counterstained with hematoxylin.

Techniques: Expressing, Comparison, Single Cell, Control, Clinical Proteomics, Translocation Assay, Whisker Assay

Journal: Blood Cancer Discovery

Article Title: CD70-Targeting CAR NK Cells Overcome BCMA Downregulation and Improve Survival in High-risk Multiple Myeloma Models

doi: 10.1158/2643-3230.BCD-25-0130

Figure Lengend Snippet: Phenotypic characterization of CD70 expression in patients with multiple myeloma. A, Bone marrow aspirates from 30 patients with multiple myeloma were stained with anti-CD70 and anti-BCMA antibodies and assayed by flow cytometry. The percentage of positive cells from the FSC/SSC/Single cells/Live-Dead/CD3 − /CD19 − /CD20 − /CD14 − /CD138+ population is plotted, with each dot representing one patient sample. The gating strategy is shown in Supplementary Fig. S3. B, The percentage of positive expression (circle size) and the robust z -score calculated from the mean fluorescence intensity (color) for CD70, BCMA, CD38, CS1, CD56, and CD45 proteins from the same population were plotted in a dot plot for each of the patient samples in ( A ). C, An optimized stochastic neighbor embedding (opt-SNE) plot was generated for each marker in the CD138 + , CD3 − , CD19/20 − , and CD14 − populations from an example patient with amp 1q and loss of one copy of TP53 . Representative images of IHC CD70 staining of the gingiva ( D ) and bone marrow ( E ) clot of a patient with high-grade myeloma. F, CD70 staining of the humerus of a patient who had not responded to the BCMA antibody–drug conjugate belantamab mafodotin. G, CD70 staining from the bone marrow of a patient without multiple myeloma as a control. Scale bar, 100 μm.

Article Snippet: The CD70 antibody (Cell Signaling Technology, clone e3Q1A, cat. #69209S) was used at a 1:50 dilution, incubated for 15 minutes at room temperature, and subsequently detected using the BOND Polymer Refine Detection kit (Leica Biosystems, cat. #DS9800) with diaminobenzidine as the chromogen and counterstained with hematoxylin.

Techniques: Expressing, Staining, Flow Cytometry, Fluorescence, Generated, Marker, Control

Journal: Blood Cancer Discovery

Article Title: CD70-Targeting CAR NK Cells Overcome BCMA Downregulation and Improve Survival in High-risk Multiple Myeloma Models

doi: 10.1158/2643-3230.BCD-25-0130

Figure Lengend Snippet: Armoring NK cells with CAR27/IL-15 results in enhanced antitumor activity against multiple myeloma. A, Schematic of the retroviral vector used to transduce CB-NK cells. B, Flow cytometry histogram assay of CD70 surface protein levels in NCI-H929 (blue) and MM.1S (magenta) cells. C, 51 Cr release assay of NT or CAR27/IL-15 NK cells against CD70 + MM.1S or ( D ) CD70 − NCI-H929 tumor cells at different E:T ratios and measured 4 hours after coincubation ( n = 3). E, MM.1S tumor cells transduced to express mKATE were cultured alone or with NT, IL-15, or CAR27/IL-15 NK cells. The number of MM.1S cells was measured over time with sequential images from the Incucyte machine. Representative images from 0 Hours (baseline) and after 24 Hours after coculture are shown. White bar, 400 μm. F, The percentage of initial MM.1S cells from panel ( E ) is plotted for each group over 30 hours. Bar graph (right) shows the AUC analysis. G, The Incucyte killing assay was repeated for NT and CAR27/IL-15 NK cells against the CD70-positive U266B1 myeloma cell line. Bar graph (right) shows the AUC analysis. Data are represented as mean ± SD. Data for the AUC graphs are represented as mean ± SEM. The P values were determined by two-way ANOVA with Sidak’s multiple comparisons ( C ), one-way ANOVA with Tukey multiple comparison ( F ), and unpaired t test ( G ). ***, P ≤ 0.001. ICD, intracellular domain; LTR, long terminal repeats; TMD, transmembrane domain.

Article Snippet: The CD70 antibody (Cell Signaling Technology, clone e3Q1A, cat. #69209S) was used at a 1:50 dilution, incubated for 15 minutes at room temperature, and subsequently detected using the BOND Polymer Refine Detection kit (Leica Biosystems, cat. #DS9800) with diaminobenzidine as the chromogen and counterstained with hematoxylin.

Techniques: Activity Assay, Retroviral, Plasmid Preparation, Transduction, Flow Cytometry, Release Assay, Cell Culture, Comparison

Journal: Blood Cancer Discovery

Article Title: CD70-Targeting CAR NK Cells Overcome BCMA Downregulation and Improve Survival in High-risk Multiple Myeloma Models

doi: 10.1158/2643-3230.BCD-25-0130

Figure Lengend Snippet: In vivo anti-myeloma activity of CD70-targeting CAR NK cells. A, Mice were first injected with MM.1S tumor cells and subsequently treated (day 0) with no additional cells (tumor alone), NT NK cells, CAR27/IL-15 NK cells, CAR27 NK cells without IL-15 (CAR27), and NK cells transduced to express only IL-15 (IL-15 NK). B, BLI was obtained weekly until day 54. Different radiance scales were used for early (days 0–14) and late (days 21–54) imaging due to signal intensities spanning several orders of magnitude. An ‘X’ denotes that all mice in the group have died. C, BLI signal for individual mice plotted over days post-CAR NK cell treatment. D, Percentage of human CD45 + cells (NK cells) detected in the blood at day 12 after NK cell infusion. Only three of the five mice per group were bled for this analysis. E, Kaplan–Meier survival plot. P value significance is denoted for the following comparisons: blue asterisks: NT NK vs. CAR27/IL-15 NK; green asterisks: CAR27 NK vs. CAR27/IL-15 NK; and magenta asterisks: IL-15 NK vs. CAR27/IL-15 NK. F, Weight of the mice in grams over time. Data are represented as mean ± SD. P values were calculated using the log-rank test ( E ). **, P ≤ 0.01.

Article Snippet: The CD70 antibody (Cell Signaling Technology, clone e3Q1A, cat. #69209S) was used at a 1:50 dilution, incubated for 15 minutes at room temperature, and subsequently detected using the BOND Polymer Refine Detection kit (Leica Biosystems, cat. #DS9800) with diaminobenzidine as the chromogen and counterstained with hematoxylin.

Techniques: In Vivo, Activity Assay, Injection, Imaging

Journal: Blood Cancer Discovery

Article Title: CD70-Targeting CAR NK Cells Overcome BCMA Downregulation and Improve Survival in High-risk Multiple Myeloma Models

doi: 10.1158/2643-3230.BCD-25-0130

Figure Lengend Snippet: Loss of BCMA does not affect the anti-myeloma activity of CAR27/IL-15 NK cells. A, Whole-cell lysates from K562 (negative control), MM.1S wild-type (WT), and MM.1S TNFRSF17 KO cells (KO) were analyzed by Western blotting for BCMA expression. β-actin served as the loading control. A representative blot is shown. B, TNFRSF17 KO efficiency analyzed by flow cytometry. C, CD70 expression of MM.1S WT and MM.1S TNFRSF17 KO tumor cells. D, 51 Cr release assay of NT NK cells or CAR27/IL-15 NK cells against MM.1S TNFRSF17 KO cells. E, Incucyte real-time killing assay of MM.1S TNFRSF17 KO tumor cells by NT NK, IL-15 NK, and CAR27/IL-15 NK cells. Bar graph (right) shows the AUC analysis. Data are represented as mean ± SD. Data for the AUC graph are represented as mean ± SEM. The P values were determined by two-way ANOVA with Sidak’s multiple comparisons ( D ) and one-way ANOVA with Tukey multiple comparisons ( E ). ***, P ≤ 0.001.

Article Snippet: The CD70 antibody (Cell Signaling Technology, clone e3Q1A, cat. #69209S) was used at a 1:50 dilution, incubated for 15 minutes at room temperature, and subsequently detected using the BOND Polymer Refine Detection kit (Leica Biosystems, cat. #DS9800) with diaminobenzidine as the chromogen and counterstained with hematoxylin.

Techniques: Activity Assay, Negative Control, Western Blot, Expressing, Control, Flow Cytometry, Release Assay

Journal: Frontiers in Immunology

Article Title: Single-cell and bulk transcriptomics reveal a CD8 + T-cell gene signature predicting prognosis in diffuse large B-cell lymphoma

doi: 10.3389/fimmu.2025.1685541

Figure Lengend Snippet: Validation cohort for predicting the risk signature of DLBCL survival based on the discovery cohort. (A) Expression of CD69 on infiltrating CD8 + T cells in DLBCL (400X). CD69 (red), CD8 (green), DAPI (blue). (B) Kaplan–Meier curves of OS in DLBCL patients with CD69 + /CD8 + and CD69 + /CD8 + . Cases were classified as CD69 + /CD8 + when ≥10% of infiltrating CD8 + T cells expressed CD69. (C) Expression of CD70 on infiltrating CD8 + T cells in DLBCL (400X). CD70 (green), CD8 (red), DAPI (blue). (D) Kaplan–Meier curves of OS in DLBCL patients with CD70 + /CD8 + and CD70 + /CD8 + . Cases were classified as CD70 + /CD8 + when ≥10% of infiltrating CD8 + T cells expressed CD70. (E) The Kaplan-Meier OS curve of the validation cohort (this work. (n=66)) patients between low risk group (n=34) and high risk group (n=32). This work samples were stratified by risk score. (F) Univariate Cox regression analysis of Risk Score: high risk, IPI: low-mid, IPI: mid-high and IPI: high in this work. (G) The Kaplan-Meier OS curve of the validation cohort ( GSE181063 (n=773)) patients between low risk group (n=387) and high risk group (n=386). GSE181063 samples were stratified by risk score. (H) Univariate Cox regression analysis of Risk Score: high risk, IPI: low-mid, IPI: mid-high and IPI: high in GSE181063 . (I) The Kaplan-Meier OS curve of the validation cohort ( GSE117556 (n=469)) patients between low risk group (n=235) and high risk group (n=234). GSE117556 samples were stratified by risk score. (J) Univariate Cox regression analysis of Risk Score: high risk, IPI: low-mid, IPI: mid-high and IPI: high in GSE117556 . Log-rank tests were used to derive p-values for comparisons between two groups.

Article Snippet: The primary antibodies are as follows: CD69 Polyclonal antibody (Proteintech, 10803-1-AP), CD70 Monoclonal antibody (Proteintech, 67749-1-Ig), CD8a Monoclonal antibody (Proteintech, 66868-1-Ig), Anti-CD8 alpha antibody (Abcam, ab93278).

Techniques: Biomarker Discovery, Expressing