Journal: bioRxiv

Article Title: Microengineered transplantation of human solid tumors for in vitro studies of CAR T immunotherapy

doi: 10.1101/2025.04.25.650709

Figure Lengend Snippet: a, Visualization of the interacting pairs of ITGAL-ICAM1 and CD38-PECAM1 in the meso-tumor model (left) and violin plots comparing the expression of interacting genes of interest mediating the crosstalk between CAR T cells and endothelial cells (right). b, Experimental timeline for CAR T cell infusion and drug treatment. c, Representative fluorescence micrographs of single meso-tumors infused with meso-CAR T cells without drug treatment (Untreated), treated with Daratumumab (0.5 or 10 μg/ml), or IgG isotype control antibody (10 μg/ml IgG). Blood vessels are not shown in these images. Scale bars, 250 μm. d,e, Quantification of T cell area ( d ) and normalized tumor area ( e ) over time. Data are presented as mean ± SEM (n ≥ 3). CAR T cells derived from one healthy donor were tested.

Article Snippet: The human CD38 inhibitor - Daratumumab (HY-P9915, MedChemExpress) and the lymphotoxin β receptor IgG fusion protein - Baminercept (HY-P99459, MedChemExpress) were used to inhibit the interactions between CD38 and its ligand PECAM1 and between lymphotoxin β and its receptor, respectively.

Techniques: Expressing, Fluorescence, Control, Derivative Assay

Journal: iScience

Article Title: CD38 is a key mediator of NAD + depletion in the brain of ZIKV-infected mice

doi: 10.1016/j.isci.2025.114018

Figure Lengend Snippet: CD38 expression and activity increase at late stages of ZIKV infection and correlate with NAD + decline in the brain (A) Total NADase activity measured in the brains of ZIKV-infected and mock-injected mice over the course of infection, showing significant increases from 18 dpi onward ( n ≥ 7 mice per group). (B) Overlay of NADase activity (red line) and NAD + levels (gray line), both relative to mock controls (dashed line), showing an inverse temporal association. (C–H) Relative mRNA expression of Sarm1 , Cd157 , and Cd38 , respectively, in the brains of ZIKV-infected and control mice ( n ≥ 4 mice per group). (D, F, H) Overlays of mRNA expression profiles of Sarm1 (D), Cd157 (F), and Cd38 (H) with NAD + levels (gray line) and ZIKV genomic RNA (yellow line), indicating that Cd38 induction temporally coincides with NAD + decline, while Sarm1 and Cd157 do not. (I) Linear regression shows a positive correlation between total NADase activity and Cd38 mRNA expression ( n = 50). (J) CD38-dependent NADase activity, calculated as the fraction inhibited by the specific CD38 inhibitor 78c ( n ≥ 6 mice per group). (K) CD38-independent NADase activity, which remains low and unchanged during infection ( n ≥ 6 mice per group). (L) On the right, representative Western blot of CD38 protein expression in brain extracts at 24 dpi, with α-tubulin as loading control (representative bands from the same experiment shown in the full blot in ). On the left, quantification of the Western blot bands’ intensities (CD38/α-tubulin) relative to mock ( n ≥ 4 mice per group). Data in panels A, C, E, G, J, K, and L are presented as mean ± SD; panels B, D, F, and H as mean ± SEM (shaded area). Statistical significance was determined by unpaired Student’s t test or Mann–Whitney test, as appropriate. ∗ p ≤ 0.05; ∗∗ p ≤ 0.01; ∗∗∗ p ≤ 0.001.

Article Snippet: Proteins were separated by electrophoresis on 15% SDS–polyacrylamide gels (SDS-PAGE), transferred to nitrocellulose membranes (Bio-Rad, California, USA), and probed with primary antibodies against CD38 (AF4947, R&D Systems, Minnesota, USA) or NAMPT (AG-20A-0034-C050, AdipoGen Life Sciences, California, USA), using concentrations recommended by the manufacturers and previously validated in-house.

Techniques: Expressing, Activity Assay, Infection, Injection, Control, Western Blot, MANN-WHITNEY

Journal: iScience

Article Title: CD38 is a key mediator of NAD + depletion in the brain of ZIKV-infected mice

doi: 10.1016/j.isci.2025.114018

Figure Lengend Snippet: CD38 inhibition prevents NAD + depletion in the brains of ZIKV-infected mice (A) Schematic representation of the experimental design. Neonatal mice were subcutaneously infected with ZIKV at postnatal day 3 (P3). At 21 days post-infection (dpi), animals received a unilateral intracerebroventricular (i.c.v.) injection of the CD38-blocking antibody Ab68 (5.76 μg) or vehicle (Veh), and brains were collected at 24 dpi for analysis. (B) NAD + hydrolase activity in brain tissue. (C) Quantification of total NAD + levels in brain tissue. Data are presented as mean ± SD. Statistical analyses were performed using an unpaired Student’s t test ( n ≥ 7 mice per group). ∗p ≤ 0.05; ∗∗∗∗p ≤ 0.0001.

Article Snippet: Proteins were separated by electrophoresis on 15% SDS–polyacrylamide gels (SDS-PAGE), transferred to nitrocellulose membranes (Bio-Rad, California, USA), and probed with primary antibodies against CD38 (AF4947, R&D Systems, Minnesota, USA) or NAMPT (AG-20A-0034-C050, AdipoGen Life Sciences, California, USA), using concentrations recommended by the manufacturers and previously validated in-house.

Techniques: Inhibition, Infection, Injection, Blocking Assay, Activity Assay

Journal: iScience

Article Title: CD38 is a key mediator of NAD + depletion in the brain of ZIKV-infected mice

doi: 10.1016/j.isci.2025.114018

Figure Lengend Snippet: NAMPT is induced in the brain of ZIKV-infected mice (A) Relative mRNA expression of Nampt in the brains of ZIKV-infected and mock-injected mice across time points post-infection ( n ≥ 4 mice per group). (B) Overlay of Nampt mRNA expression (blue line), total NADase activity (red line), NAD + levels (gray line), and ZIKV genomic RNA (yellow line), all relative to mock controls (dashed line). (C–F) Correlation analyses between Nampt mRNA expression and (C) ZIKV genomic RNA, (D) Parp12 , (E) Parp10 , and (F) Cd38 mRNA expression. Nampt shows a strong correlation with viral load and early-induced Parps , but a weak correlation with Cd38 . (G) Representative Western blot of NAMPT protein expression in the brains of ZIKV-infected and mock-injected mice at 24 days post-infection (dpi; representative bands from the same experiment shown in the full blot in ).. HPRT was used as a loading control. The right panel shows quantification of NAMPT protein levels (NAMPT/HPRT ratio), normalized to mock controls ( n ≥ 4 mice per group). Data in panels A and G are presented as mean ± SD; panel B as mean ± SEM (shaded area). Correlations were assessed by linear regression analysis. Statistical analyses were performed using an unpaired Student’s t test or Mann–Whitney test, as appropriate. ∗ p ≤ 0.05; ∗∗ p ≤ 0.01; ∗∗∗ p ≤ 0.001.

Article Snippet: Proteins were separated by electrophoresis on 15% SDS–polyacrylamide gels (SDS-PAGE), transferred to nitrocellulose membranes (Bio-Rad, California, USA), and probed with primary antibodies against CD38 (AF4947, R&D Systems, Minnesota, USA) or NAMPT (AG-20A-0034-C050, AdipoGen Life Sciences, California, USA), using concentrations recommended by the manufacturers and previously validated in-house.

Techniques: Infection, Expressing, Injection, Activity Assay, Western Blot, Control, MANN-WHITNEY

Journal: iScience

Article Title: CD38 is a key mediator of NAD + depletion in the brain of ZIKV-infected mice

doi: 10.1016/j.isci.2025.114018

Figure Lengend Snippet: Proinflammatory cytokine expression precedes CD38 induction in the brains of ZIKV-infected mice (A, C, E) Relative mRNA expression of Il6 and Tnf (linear scale), and Ccl5/Rantes (Log 10 -transformed) in the brains of ZIKV-infected and mock-injected mice across time points post-infection ( n ≥ 3 mice per group). All three inflammatory mediators were significantly upregulated during the early and mid-stages of infection. (B, D, F) Overlay of Il6 (B), Tnf (D), and Rantes – log 10 scale (F) mRNA expression profiles (purple line) with Cd38 mRNA (red line), NAD + levels (gray line), and ZIKV genomic RNA (yellow line), all relative to mock controls (dashed line). (G) Brain IL-6 protein levels determined by ELISA ( n ≥ 5 mice per group). The temporal pattern shows that cytokine and chemokine induction precede Cd38 expression, suggesting that neuroinflammation may contribute to the upregulation of CD38. Data in panels A, C, and E are presented as mean ± SD; panels B, D, and F as mean ± SEM (shaded area). Statistical analyses were performed using an unpaired Student’s t test or Mann–Whitney test, as appropriate. ∗ p ≤ 0.05; ∗∗ p ≤ 0.01; ∗∗∗ p ≤ 0.001.

Article Snippet: Proteins were separated by electrophoresis on 15% SDS–polyacrylamide gels (SDS-PAGE), transferred to nitrocellulose membranes (Bio-Rad, California, USA), and probed with primary antibodies against CD38 (AF4947, R&D Systems, Minnesota, USA) or NAMPT (AG-20A-0034-C050, AdipoGen Life Sciences, California, USA), using concentrations recommended by the manufacturers and previously validated in-house.

Techniques: Expressing, Infection, Transformation Assay, Injection, Enzyme-linked Immunosorbent Assay, MANN-WHITNEY

Journal: iScience

Article Title: CD38 is a key mediator of NAD + depletion in the brain of ZIKV-infected mice

doi: 10.1016/j.isci.2025.114018

Figure Lengend Snippet: Infiltrating immune cells contribute to increased CD38 expression in the brains of ZIKV-infected mice (A) On the left, representative dot plots show the gating strategy used to identify CD45 lo CD11b + (putative resting microglia), CD45 hi CD11b + (infiltrating myeloid cells), and CD45 + CD11b − (lymphoid cells) populations. On the right, graphs showing the frequency of each population in ZIKV-infected and mock-injected mice ( n ≥ 5 mice per group). (B) Representative dot plots and quantification of CD11b + TMEM119 + , CD11b + TMEM119 + , and CD11b + TMEM119 - populations in the brains of infected and control mice ( n ≥ 6 mice per group), with the respective graphs showing the frequency of each population. (C–E) Representative histograms and quantification of CD38 expression (median fluorescence intensity, MFI) in CD11b + TMEM119 + (C) CD11b − TMEM119 + (D), and CD11b + TMEM119 - (E) populations. (F and G) Gating and quantification of CD3 + T cells (F) and corresponding CD38 expression (G). (H and I) Gating and quantification of CD19 + B cells (H) and corresponding CD38 expression (I). All graphs represent mean ± SD. Gating was based on negative controls; histogram quantification was performed using MFI, and curves were normalized to unit area. Statistical analyses were performed using an unpaired Student’s t test or Mann–Whitney test, as appropriate. ∗ p ≤ 0.05; ∗∗ p ≤ 0.01; ∗∗∗∗ p ≤ 0.0001.

Article Snippet: Proteins were separated by electrophoresis on 15% SDS–polyacrylamide gels (SDS-PAGE), transferred to nitrocellulose membranes (Bio-Rad, California, USA), and probed with primary antibodies against CD38 (AF4947, R&D Systems, Minnesota, USA) or NAMPT (AG-20A-0034-C050, AdipoGen Life Sciences, California, USA), using concentrations recommended by the manufacturers and previously validated in-house.

Techniques: Expressing, Infection, Injection, Control, Fluorescence, MANN-WHITNEY

Journal: Cell

Article Title: Elevated Calprotectin and Abnormal Myeloid Cell Subsets Discriminate Severe from Mild COVID-19

doi: 10.1016/j.cell.2020.08.002

Figure Lengend Snippet:

Article Snippet: CD38 , Fluidigm , Pro# 3167001B.

Techniques: Recombinant, Reverse Transcription, SYBR Green Assay, Staining, Functional Assay, Software

Journal: Cell Reports Methods

Article Title: Generation, expansion, gene delivery, and single-cell profiling in rhesus macaque plasma B cells

doi: 10.1016/j.crmeth.2024.100878

Figure Lengend Snippet:

Article Snippet: anti-CD38 FITC clone: OKT10 , Caprico Biotechnologies , 100815.

Techniques: Enzyme-linked Immunospot, Isolation, Enzyme-linked Immunosorbent Assay, Recombinant, Software

Journal: Nature Communications

Article Title: CD200R1-CD200 checkpoint inhibits phagocytosis differently from SIRPα-CD47 to suppress tumor growth

doi: 10.1038/s41467-025-60456-3

Figure Lengend Snippet: a Flow cytometry analysis of CD200 (top) or tumor antigens (CD20, CD38, CD123, DLL3 and SLAMF7; bottom) on various human tumor cell lines. Red curves, CD200 mAb or tumor antigen-specific mAbs. Filled curves, Ctrl mAbs. b As per Fig. , except using IL-4-primed human blood monocyte-derived macrophages and human tumor cells in the presence of samalizumab (human IgG1, Fc-silent) or Ctrl mAb MOPC21 (human IgG1, Fc-silent). IgG opsonization was performed using CD20 mAb rituximab (SLVL, 721.221), CD38 mAb daratumumab (NCI-H929), CD123 mAb talacotuzumab (KG-1a), DLL3 mAb rovalpituzumab (NCI-H209), or SLAMF7 mAb elotuzumab (SK-MEL-28) ( n = 3 or 4). c As per Fig. 5b, except using the indicated cell lines and samalizumab (human IgG1, Fc-silent), CD47 mAb B6H12 (human IgG1, Fc-silent), or Ctrl mAb MOPC21 (human IgG1, Fc-silent). Tumor cells were opsonized as detailed for Fig. 5b, ( n = 3). d –f Subcutaneous injection of SLVL cells in NSG mice, followed by intraperitoneal injection of rituximab (mouse IgG2a version) combined with samalizumab or Ctrl mAb every 2 days, ( n = 8). d Schematic representation of the experimental workflow. e Tumor volume over time. f Tumor weight. g –i Subcutaneous injection of 721.221 cells in NSG mice, followed by intraperitoneal injection of rituximab (mouse IgG2a version) combined with samalizumab or Ctrl mAbs every 2 days, ( n = 10). g Schematic representation of the experimental workflow. h Tumor volume over time. i Tumor weight. Data are from three to four ( a, b ), three ( c ), or two ( d-i ) independent experiments. Each symbol represents one human sample or one mouse. Data are presented as mean ± s.e.m. Statistical analysis: two-tailed t-test ( f , i ), with multiple comparisons ( b, c , e , h ). ns, not significant. See also Supplementary Fig. .

Article Snippet: For cell opsonization, the following mAbs were used: Tac mAb 7G7 (BioXCell); human CD20 mAb rituximab biosimilar (BioXCell); human CD123 mAb talacotuzumab (MedChemExpress, Princeton, NJ); human CD38 mAb daratumumab (MedChemExpress); human DLL3 mAb rovalpituzumab (MedChemExpress).

Techniques: Flow Cytometry, Derivative Assay, Injection, Two Tailed Test