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Fig. 5. Functional activity of havPD-1 EVs in cell-based assays. (a) Neutralization of PD-L1 in a cell assay by havPD-1 EVs in comparison with a clinical control, Atezolizumab. (b) Mixed lymphocyte reaction assay. Supernatants were measured for IFN-γ production by <t>ELISA</t> (n = 8). (c) Tetanus toxoids recall assay. Super natants were measured for IFN-γ production by ELISA (n = 8) (d) Antigen-dependent cell-mediated cytotoxicity assay (n = 8). (e) Complement dependent cyto toxicity assay (n = 8).
Ifnγ With Elisa, supplied by R&D Systems, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Fig. 5. Functional activity of havPD-1 EVs in cell-based assays. (a) Neutralization of PD-L1 in a cell assay by havPD-1 EVs in comparison with a clinical control, Atezolizumab. (b) Mixed lymphocyte reaction assay. Supernatants were measured for IFN-γ production by <t>ELISA</t> (n = 8). (c) Tetanus toxoids recall assay. Super natants were measured for IFN-γ production by ELISA (n = 8) (d) Antigen-dependent cell-mediated cytotoxicity assay (n = 8). (e) Complement dependent cyto toxicity assay (n = 8).
Human Ifn Gamma Quantikine Elisa Kit, supplied by R&D Systems, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Representation of normalized parameters related to immune CD4 + (a, b) and CD8 + (c, d) T cell populations before and after stimulation with UV‐inactivated measles (a, c) or rubella (b, d) virus with <t>relative</t> <t>IFN‐γ</t> induction (e, f). Nonstimulated samples (blue) are linked to the stimulated counterparts (measles, red; rubella, green) through connection lines. Among both populations, Naïve, Central Memory (CM), Effector Memory (EM), and Terminally Differentiated Effector Memory (TEMRA) cells were analyzed. Moreover, among CD4 + cells, T helper (Th) 1, 2, and 17 were analyzed. Results were expressed as the variation in the population percentage (with respect to CD4 + and CD8 + cells). Statistical significance was assessed using the two‐tailed χ 2 test. The p values are reported in the figures, where * stands for p < 0.05 and ** for p < 0.01. No differences were reported in the CD4 + and CD8 + populations, as well as in IFN‐γ induction, between the nonstimulated and measles‐stimulated groups.
Human Ifn γ Quantikine, supplied by R&D Systems, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Representation of normalized parameters related to immune CD4 + (a, b) and CD8 + (c, d) T cell populations before and after stimulation with UV‐inactivated measles (a, c) or rubella (b, d) virus with <t>relative</t> <t>IFN‐γ</t> induction (e, f). Nonstimulated samples (blue) are linked to the stimulated counterparts (measles, red; rubella, green) through connection lines. Among both populations, Naïve, Central Memory (CM), Effector Memory (EM), and Terminally Differentiated Effector Memory (TEMRA) cells were analyzed. Moreover, among CD4 + cells, T helper (Th) 1, 2, and 17 were analyzed. Results were expressed as the variation in the population percentage (with respect to CD4 + and CD8 + cells). Statistical significance was assessed using the two‐tailed χ 2 test. The p values are reported in the figures, where * stands for p < 0.05 and ** for p < 0.01. No differences were reported in the CD4 + and CD8 + populations, as well as in IFN‐γ induction, between the nonstimulated and measles‐stimulated groups.
Human Ifn γ Quantikine R D Systems Minneapolis Minn, supplied by R&D Systems, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Ebola, Nipah, and Andes viruses each exert different effects on hPSC-derived ECs A) Experimental summary. h: hour. B) Replication of Andes, Nipah, and Ebola viruses in hPSC-derived artery and vein ECs, as assayed by qPCR for viral genomes in the culture media. Statistics: unpaired t-test. Error bars: SEM. **P<0.01. n.s.: not significant. †: extensive cell death. C) Bulk RNA-seq of interferon and interferon-stimulated gene expression in hPSC-derived artery and vein ECs 6, 12, 24, and 48 hours after infection with Sendai, Andes, Nipah, and Ebola viruses. Fold change relative to uninfected cells is depicted. D) Bulk RNA-seq of inflammatory cytokine gene expression in hPSC-derived artery and vein ECs 6, 12, 24, and 48 hours after infection with Sendai, Andes, Nipah, and Ebola viruses. Fold change relative to uninfected cells is depicted. E) Summary of the present study. F) Bulk-RNA-seq of hPSC-derived artery ECs 6, 12, 24, and 48 hours after infection with Ebola, Andes, and Sendai viruses, or left uninfected (mock control). Error bars: SEM. G) <t>IFNβ</t> protein secretion by hPSC-derived artery ECs after 24 or 48 hours of infection by Ebola, Andes, and Sendai viruses, or left uninfected (mock control), as measured by <t>ELISA.</t> Statistics: unpaired t-test. **P<0.01. H) Bulk-RNA-seq of hPSC-derived artery ECs 6, 12, 24, and 48 hours after infection with Ebola, Andes, and Sendai viruses, or left uninfected (mock control). Error bars: SEM. Related to Figures S7 and S8.
Human Ifnβ Quantikine Quickit Elisa Kit, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Ebola, Nipah, and Andes viruses each exert different effects on hPSC-derived ECs A) Experimental summary. h: hour. B) Replication of Andes, Nipah, and Ebola viruses in hPSC-derived artery and vein ECs, as assayed by qPCR for viral genomes in the culture media. Statistics: unpaired t-test. Error bars: SEM. **P<0.01. n.s.: not significant. †: extensive cell death. C) Bulk RNA-seq of interferon and interferon-stimulated gene expression in hPSC-derived artery and vein ECs 6, 12, 24, and 48 hours after infection with Sendai, Andes, Nipah, and Ebola viruses. Fold change relative to uninfected cells is depicted. D) Bulk RNA-seq of inflammatory cytokine gene expression in hPSC-derived artery and vein ECs 6, 12, 24, and 48 hours after infection with Sendai, Andes, Nipah, and Ebola viruses. Fold change relative to uninfected cells is depicted. E) Summary of the present study. F) Bulk-RNA-seq of hPSC-derived artery ECs 6, 12, 24, and 48 hours after infection with Ebola, Andes, and Sendai viruses, or left uninfected (mock control). Error bars: SEM. G) <t>IFNβ</t> protein secretion by hPSC-derived artery ECs after 24 or 48 hours of infection by Ebola, Andes, and Sendai viruses, or left uninfected (mock control), as measured by <t>ELISA.</t> Statistics: unpaired t-test. **P<0.01. H) Bulk-RNA-seq of hPSC-derived artery ECs 6, 12, 24, and 48 hours after infection with Ebola, Andes, and Sendai viruses, or left uninfected (mock control). Error bars: SEM. Related to Figures S7 and S8.
Quantikine Human Ifn β Elisa Kit, supplied by R&D Systems, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Ebola, Nipah, and Andes viruses each exert different effects on hPSC-derived ECs A) Experimental summary. h: hour. B) Replication of Andes, Nipah, and Ebola viruses in hPSC-derived artery and vein ECs, as assayed by qPCR for viral genomes in the culture media. Statistics: unpaired t-test. Error bars: SEM. **P<0.01. n.s.: not significant. †: extensive cell death. C) Bulk RNA-seq of interferon and interferon-stimulated gene expression in hPSC-derived artery and vein ECs 6, 12, 24, and 48 hours after infection with Sendai, Andes, Nipah, and Ebola viruses. Fold change relative to uninfected cells is depicted. D) Bulk RNA-seq of inflammatory cytokine gene expression in hPSC-derived artery and vein ECs 6, 12, 24, and 48 hours after infection with Sendai, Andes, Nipah, and Ebola viruses. Fold change relative to uninfected cells is depicted. E) Summary of the present study. F) Bulk-RNA-seq of hPSC-derived artery ECs 6, 12, 24, and 48 hours after infection with Ebola, Andes, and Sendai viruses, or left uninfected (mock control). Error bars: SEM. G) <t>IFNβ</t> protein secretion by hPSC-derived artery ECs after 24 or 48 hours of infection by Ebola, Andes, and Sendai viruses, or left uninfected (mock control), as measured by <t>ELISA.</t> Statistics: unpaired t-test. **P<0.01. H) Bulk-RNA-seq of hPSC-derived artery ECs 6, 12, 24, and 48 hours after infection with Ebola, Andes, and Sendai viruses, or left uninfected (mock control). Error bars: SEM. Related to Figures S7 and S8.
Ifn λ3 Il 28b, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Ebola, Nipah, and Andes viruses each exert different effects on hPSC-derived ECs A) Experimental summary. h: hour. B) Replication of Andes, Nipah, and Ebola viruses in hPSC-derived artery and vein ECs, as assayed by qPCR for viral genomes in the culture media. Statistics: unpaired t-test. Error bars: SEM. **P<0.01. n.s.: not significant. †: extensive cell death. C) Bulk RNA-seq of interferon and interferon-stimulated gene expression in hPSC-derived artery and vein ECs 6, 12, 24, and 48 hours after infection with Sendai, Andes, Nipah, and Ebola viruses. Fold change relative to uninfected cells is depicted. D) Bulk RNA-seq of inflammatory cytokine gene expression in hPSC-derived artery and vein ECs 6, 12, 24, and 48 hours after infection with Sendai, Andes, Nipah, and Ebola viruses. Fold change relative to uninfected cells is depicted. E) Summary of the present study. F) Bulk-RNA-seq of hPSC-derived artery ECs 6, 12, 24, and 48 hours after infection with Ebola, Andes, and Sendai viruses, or left uninfected (mock control). Error bars: SEM. G) <t>IFNβ</t> protein secretion by hPSC-derived artery ECs after 24 or 48 hours of infection by Ebola, Andes, and Sendai viruses, or left uninfected (mock control), as measured by <t>ELISA.</t> Statistics: unpaired t-test. **P<0.01. H) Bulk-RNA-seq of hPSC-derived artery ECs 6, 12, 24, and 48 hours after infection with Ebola, Andes, and Sendai viruses, or left uninfected (mock control). Error bars: SEM. Related to Figures S7 and S8.
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Ebola, Nipah, and Andes viruses each exert different effects on hPSC-derived ECs A) Experimental summary. h: hour. B) Replication of Andes, Nipah, and Ebola viruses in hPSC-derived artery and vein ECs, as assayed by qPCR for viral genomes in the culture media. Statistics: unpaired t-test. Error bars: SEM. **P<0.01. n.s.: not significant. †: extensive cell death. C) Bulk RNA-seq of interferon and interferon-stimulated gene expression in hPSC-derived artery and vein ECs 6, 12, 24, and 48 hours after infection with Sendai, Andes, Nipah, and Ebola viruses. Fold change relative to uninfected cells is depicted. D) Bulk RNA-seq of inflammatory cytokine gene expression in hPSC-derived artery and vein ECs 6, 12, 24, and 48 hours after infection with Sendai, Andes, Nipah, and Ebola viruses. Fold change relative to uninfected cells is depicted. E) Summary of the present study. F) Bulk-RNA-seq of hPSC-derived artery ECs 6, 12, 24, and 48 hours after infection with Ebola, Andes, and Sendai viruses, or left uninfected (mock control). Error bars: SEM. G) <t>IFNβ</t> protein secretion by hPSC-derived artery ECs after 24 or 48 hours of infection by Ebola, Andes, and Sendai viruses, or left uninfected (mock control), as measured by <t>ELISA.</t> Statistics: unpaired t-test. **P<0.01. H) Bulk-RNA-seq of hPSC-derived artery ECs 6, 12, 24, and 48 hours after infection with Ebola, Andes, and Sendai viruses, or left uninfected (mock control). Error bars: SEM. Related to Figures S7 and S8.
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Image Search Results


Fig. 5. Functional activity of havPD-1 EVs in cell-based assays. (a) Neutralization of PD-L1 in a cell assay by havPD-1 EVs in comparison with a clinical control, Atezolizumab. (b) Mixed lymphocyte reaction assay. Supernatants were measured for IFN-γ production by ELISA (n = 8). (c) Tetanus toxoids recall assay. Super natants were measured for IFN-γ production by ELISA (n = 8) (d) Antigen-dependent cell-mediated cytotoxicity assay (n = 8). (e) Complement dependent cyto toxicity assay (n = 8).

Journal: Bioactive materials

Article Title: Engineered extracellular vesicles for concurrent Anti-PDL1 immunotherapy and chemotherapy.

doi: 10.1016/j.bioactmat.2021.07.012

Figure Lengend Snippet: Fig. 5. Functional activity of havPD-1 EVs in cell-based assays. (a) Neutralization of PD-L1 in a cell assay by havPD-1 EVs in comparison with a clinical control, Atezolizumab. (b) Mixed lymphocyte reaction assay. Supernatants were measured for IFN-γ production by ELISA (n = 8). (c) Tetanus toxoids recall assay. Super natants were measured for IFN-γ production by ELISA (n = 8) (d) Antigen-dependent cell-mediated cytotoxicity assay (n = 8). (e) Complement dependent cyto toxicity assay (n = 8).

Article Snippet: After incubation for 3 days at 37 ◦C and 5% CO2, supernatants were harvested and subjected to detection of IFNγ with ELISA (R&D Systems, DIF50).

Techniques: Functional Assay, Activity Assay, Neutralization, Comparison, Control, Enzyme-linked Immunosorbent Assay, Cytotoxicity Assay

Representation of normalized parameters related to immune CD4 + (a, b) and CD8 + (c, d) T cell populations before and after stimulation with UV‐inactivated measles (a, c) or rubella (b, d) virus with relative IFN‐γ induction (e, f). Nonstimulated samples (blue) are linked to the stimulated counterparts (measles, red; rubella, green) through connection lines. Among both populations, Naïve, Central Memory (CM), Effector Memory (EM), and Terminally Differentiated Effector Memory (TEMRA) cells were analyzed. Moreover, among CD4 + cells, T helper (Th) 1, 2, and 17 were analyzed. Results were expressed as the variation in the population percentage (with respect to CD4 + and CD8 + cells). Statistical significance was assessed using the two‐tailed χ 2 test. The p values are reported in the figures, where * stands for p < 0.05 and ** for p < 0.01. No differences were reported in the CD4 + and CD8 + populations, as well as in IFN‐γ induction, between the nonstimulated and measles‐stimulated groups.

Journal: Journal of Medical Virology

Article Title: Seronegative Vaccinees May Not Benefit From Multiple Booster Doses of MMR Vaccine in Restoring Immunity

doi: 10.1002/jmv.70135

Figure Lengend Snippet: Representation of normalized parameters related to immune CD4 + (a, b) and CD8 + (c, d) T cell populations before and after stimulation with UV‐inactivated measles (a, c) or rubella (b, d) virus with relative IFN‐γ induction (e, f). Nonstimulated samples (blue) are linked to the stimulated counterparts (measles, red; rubella, green) through connection lines. Among both populations, Naïve, Central Memory (CM), Effector Memory (EM), and Terminally Differentiated Effector Memory (TEMRA) cells were analyzed. Moreover, among CD4 + cells, T helper (Th) 1, 2, and 17 were analyzed. Results were expressed as the variation in the population percentage (with respect to CD4 + and CD8 + cells). Statistical significance was assessed using the two‐tailed χ 2 test. The p values are reported in the figures, where * stands for p < 0.05 and ** for p < 0.01. No differences were reported in the CD4 + and CD8 + populations, as well as in IFN‐γ induction, between the nonstimulated and measles‐stimulated groups.

Article Snippet: To further evaluate both T and NK cell response following stimulation with UV‐inactivated measles and rubella viruses (the latter serving as a positive control), supernatants of stimulated PBMCs were analyzed for IFN‐γ and Granzyme B expression using the Human IFN‐γ Quantikine and Human Granzyme B Duoset ELISA Kits (R&D Systems, MN, USA).

Techniques: Virus, Two Tailed Test

Ebola, Nipah, and Andes viruses each exert different effects on hPSC-derived ECs A) Experimental summary. h: hour. B) Replication of Andes, Nipah, and Ebola viruses in hPSC-derived artery and vein ECs, as assayed by qPCR for viral genomes in the culture media. Statistics: unpaired t-test. Error bars: SEM. **P<0.01. n.s.: not significant. †: extensive cell death. C) Bulk RNA-seq of interferon and interferon-stimulated gene expression in hPSC-derived artery and vein ECs 6, 12, 24, and 48 hours after infection with Sendai, Andes, Nipah, and Ebola viruses. Fold change relative to uninfected cells is depicted. D) Bulk RNA-seq of inflammatory cytokine gene expression in hPSC-derived artery and vein ECs 6, 12, 24, and 48 hours after infection with Sendai, Andes, Nipah, and Ebola viruses. Fold change relative to uninfected cells is depicted. E) Summary of the present study. F) Bulk-RNA-seq of hPSC-derived artery ECs 6, 12, 24, and 48 hours after infection with Ebola, Andes, and Sendai viruses, or left uninfected (mock control). Error bars: SEM. G) IFNβ protein secretion by hPSC-derived artery ECs after 24 or 48 hours of infection by Ebola, Andes, and Sendai viruses, or left uninfected (mock control), as measured by ELISA. Statistics: unpaired t-test. **P<0.01. H) Bulk-RNA-seq of hPSC-derived artery ECs 6, 12, 24, and 48 hours after infection with Ebola, Andes, and Sendai viruses, or left uninfected (mock control). Error bars: SEM. Related to Figures S7 and S8.

Journal: bioRxiv

Article Title: A human arteriovenous differentiation roadmap reveals vein developmental mechanisms and vascular effects of viruses

doi: 10.1101/2025.10.11.681838

Figure Lengend Snippet: Ebola, Nipah, and Andes viruses each exert different effects on hPSC-derived ECs A) Experimental summary. h: hour. B) Replication of Andes, Nipah, and Ebola viruses in hPSC-derived artery and vein ECs, as assayed by qPCR for viral genomes in the culture media. Statistics: unpaired t-test. Error bars: SEM. **P<0.01. n.s.: not significant. †: extensive cell death. C) Bulk RNA-seq of interferon and interferon-stimulated gene expression in hPSC-derived artery and vein ECs 6, 12, 24, and 48 hours after infection with Sendai, Andes, Nipah, and Ebola viruses. Fold change relative to uninfected cells is depicted. D) Bulk RNA-seq of inflammatory cytokine gene expression in hPSC-derived artery and vein ECs 6, 12, 24, and 48 hours after infection with Sendai, Andes, Nipah, and Ebola viruses. Fold change relative to uninfected cells is depicted. E) Summary of the present study. F) Bulk-RNA-seq of hPSC-derived artery ECs 6, 12, 24, and 48 hours after infection with Ebola, Andes, and Sendai viruses, or left uninfected (mock control). Error bars: SEM. G) IFNβ protein secretion by hPSC-derived artery ECs after 24 or 48 hours of infection by Ebola, Andes, and Sendai viruses, or left uninfected (mock control), as measured by ELISA. Statistics: unpaired t-test. **P<0.01. H) Bulk-RNA-seq of hPSC-derived artery ECs 6, 12, 24, and 48 hours after infection with Ebola, Andes, and Sendai viruses, or left uninfected (mock control). Error bars: SEM. Related to Figures S7 and S8.

Article Snippet: Media was then thawed, and the concentration of secreted interferon-β (IFNβ) protein in the 2:1 diluted media was quantified using the Human IFNβ Quantikine QuicKit ELISA Kit (R&D Systems, QK410), as described previously and as per the manufacturer’s instructions.

Techniques: Derivative Assay, RNA Sequencing, Gene Expression, Infection, Control, Enzyme-linked Immunosorbent Assay