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Ajinomoto Althea s inks differentiation

Figure 1. Limited bone marrow homing of <t>IL15-iNKs</t> could be rescued by overexpression of CXCR4. (A) RNA-seq reveals the transcriptional level of chemotaxis-associated genes in PBNKs, iNKs, and IL15-iNKs (n = 6 for each group). Statistical signiﬁcance was determined by one-way ANOVA or Kruskal-Wallis analysis, and Tukey test was used to analyze the speciﬁc difference group by group. (B) Flow cytometry analysis of CXCR4 expression on PBNKs, iNKs, and IL15- iNKs. (C) Experimental design to evaluate CXCR4 function in bone marrow (BM) homing using IL15-iNKs. IL15-iNKs were transduced with CXCR4 or luciferase (control), then infused into NOG mice for pharmacokinetic analysis (n = 5 for each group). Two groups of mice were euthanized to obtain BM from femur at day 7 (n = 2) and day 14 (n = 3). BM was resuspended by 200 μl phosphate buffered saline (PBS) for further analysis. (D) Pharmacokinetics of iNKs by detecting CD45+ CD56+ cells in the same volume of peripheral blood (left) and BM (right) at day 7 and day 14 using ﬂow cytometry. Statistical signiﬁcance was determined by unpaired t test. Data are presented as mean ± SD (D). *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001; ns, no statistical signiﬁcance. Abbreviations: CXCR4, C-X-C chemokine receptor type 4; <t>iNK,</t> <t>iPSC-derived</t> natural killer cell; PBNK, peripheral blood NK cell.

S Inks Differentiation, supplied by Ajinomoto Althea, used in various techniques. Bioz Stars score: 94/100, based on 7 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/sf051-001/pm40312161-286-19-33?v=Ajinomoto+Althea
Average 94 stars, based on 7 article reviews

s inks differentiation - by Bioz Stars, 2026-07

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1) Product Images from "Regulatable C-X-C chemokine receptor type 4 in iPSC-derived NK cells improves bone marrow chemotaxis and targeting resident tumor."

Article Title: Regulatable C-X-C chemokine receptor type 4 in iPSC-derived NK cells improves bone marrow chemotaxis and targeting resident tumor.

Journal: Trends in biotechnology

doi: 10.1016/j.tibtech.2025.02.018

Figure 1. Limited bone marrow homing of IL15-iNKs could be rescued by overexpression of CXCR4. (A) RNA-seq reveals the transcriptional level of chemotaxis-associated genes in PBNKs, iNKs, and IL15-iNKs (n = 6 for each group). Statistical signiﬁcance was determined by one-way ANOVA or Kruskal-Wallis analysis, and Tukey test was used to analyze the speciﬁc difference group by group. (B) Flow cytometry analysis of CXCR4 expression on PBNKs, iNKs, and IL15- iNKs. (C) Experimental design to evaluate CXCR4 function in bone marrow (BM) homing using IL15-iNKs. IL15-iNKs were transduced with CXCR4 or luciferase (control), then infused into NOG mice for pharmacokinetic analysis (n = 5 for each group). Two groups of mice were euthanized to obtain BM from femur at day 7 (n = 2) and day 14 (n = 3). BM was resuspended by 200 μl phosphate buffered saline (PBS) for further analysis. (D) Pharmacokinetics of iNKs by detecting CD45+ CD56+ cells in the same volume of peripheral blood (left) and BM (right) at day 7 and day 14 using ﬂow cytometry. Statistical signiﬁcance was determined by unpaired t test. Data are presented as mean ± SD (D). *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001; ns, no statistical signiﬁcance. Abbreviations: CXCR4, C-X-C chemokine receptor type 4; iNK, iPSC-derived natural killer cell; PBNK, peripheral blood NK cell.

Figure Legend Snippet: Figure 1. Limited bone marrow homing of IL15-iNKs could be rescued by overexpression of CXCR4. (A) RNA-seq reveals the transcriptional level of chemotaxis-associated genes in PBNKs, iNKs, and IL15-iNKs (n = 6 for each group). Statistical signiﬁcance was determined by one-way ANOVA or Kruskal-Wallis analysis, and Tukey test was used to analyze the speciﬁc difference group by group. (B) Flow cytometry analysis of CXCR4 expression on PBNKs, iNKs, and IL15- iNKs. (C) Experimental design to evaluate CXCR4 function in bone marrow (BM) homing using IL15-iNKs. IL15-iNKs were transduced with CXCR4 or luciferase (control), then infused into NOG mice for pharmacokinetic analysis (n = 5 for each group). Two groups of mice were euthanized to obtain BM from femur at day 7 (n = 2) and day 14 (n = 3). BM was resuspended by 200 μl phosphate buffered saline (PBS) for further analysis. (D) Pharmacokinetics of iNKs by detecting CD45+ CD56+ cells in the same volume of peripheral blood (left) and BM (right) at day 7 and day 14 using ﬂow cytometry. Statistical signiﬁcance was determined by unpaired t test. Data are presented as mean ± SD (D). *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001; ns, no statistical signiﬁcance. Abbreviations: CXCR4, C-X-C chemokine receptor type 4; iNK, iPSC-derived natural killer cell; PBNK, peripheral blood NK cell.

Techniques Used: Over Expression, RNA Sequencing, Chemotaxis Assay, Flow Cytometry, Expressing, Transduction, Luciferase, Control, Saline, Drug discovery, Cytometry, Derivative Assay

Figure 2. Overexpression of CXCR4 affects hematopoietic differentiation of iPSC. (A) Diagram of engineering iPSC with varying levels of CXCR4 expression and their iNK differentiation. (B) Flow cytometry analysis of CXCR4 expression on edited iPSC. (C) Representative images of embryoid bodies (EBs) formed by different iPSC groups at day 9. (D) Flow cytometry analysis of hematopoietic stem and progenitor cell (HSPC) markers (CD43 and CD34) on cells isolated from EB. The gating strategy was built to exclude the isotype staining strictly. (E) Final iNK (CD56+ ) yields from CXCR4low iPSC clones (n = 3) and control iPSC clones (n = 2), demonstrated as ﬁnal iNKs from each starting iPSC cell. (F) Flow cytometry analysis of CXCR4 levels on iNKs of different groups. (G) Cytotoxicity analysis of CXCR4low iNKs and control iNKs by targeting GFP-labeled THP-1 tumor cells at a 3:1 Effector-to-Target (E:T) ratio in an IncuCyte-based functional assay. Data are presented as mean ± SD (D,E,G). Abbreviations: CXCR4, C-X-C chemokine receptor type 4; iNK, iPSC-derived natural killer cell.

Figure Legend Snippet: Figure 2. Overexpression of CXCR4 affects hematopoietic differentiation of iPSC. (A) Diagram of engineering iPSC with varying levels of CXCR4 expression and their iNK differentiation. (B) Flow cytometry analysis of CXCR4 expression on edited iPSC. (C) Representative images of embryoid bodies (EBs) formed by different iPSC groups at day 9. (D) Flow cytometry analysis of hematopoietic stem and progenitor cell (HSPC) markers (CD43 and CD34) on cells isolated from EB. The gating strategy was built to exclude the isotype staining strictly. (E) Final iNK (CD56+ ) yields from CXCR4low iPSC clones (n = 3) and control iPSC clones (n = 2), demonstrated as ﬁnal iNKs from each starting iPSC cell. (F) Flow cytometry analysis of CXCR4 levels on iNKs of different groups. (G) Cytotoxicity analysis of CXCR4low iNKs and control iNKs by targeting GFP-labeled THP-1 tumor cells at a 3:1 Effector-to-Target (E:T) ratio in an IncuCyte-based functional assay. Data are presented as mean ± SD (D,E,G). Abbreviations: CXCR4, C-X-C chemokine receptor type 4; iNK, iPSC-derived natural killer cell.

Techniques Used: Over Expression, Expressing, Flow Cytometry, Isolation, Staining, Clone Assay, Control, Labeling, Functional Assay, Derivative Assay

Figure 4. iPSC with targeted knock-in of CXCR4 at the GZMB locus demonstrate normal iNK differentiation and function. (A) Schematic view of targeted insertion of CXCR4 and BFP at GZMB locus. (B) Diagram illustrating the engineer process of CXCR4GZMB and BFPGZMB iPSC and their iNK differentiation process. (C) Representative images of EB formation of different groups of iPSC clones (upper panel). Flow cytometry analysis of hematopoietic stem and progenitor cell (HSPC)

Figure Legend Snippet: Figure 4. iPSC with targeted knock-in of CXCR4 at the GZMB locus demonstrate normal iNK differentiation and function. (A) Schematic view of targeted insertion of CXCR4 and BFP at GZMB locus. (B) Diagram illustrating the engineer process of CXCR4GZMB and BFPGZMB iPSC and their iNK differentiation process. (C) Representative images of EB formation of different groups of iPSC clones (upper panel). Flow cytometry analysis of hematopoietic stem and progenitor cell (HSPC)

Techniques Used: Knock-In, Clone Assay, Flow Cytometry

Figure 5. Regulatable CXCR4 in iPSC-derived NKs enhances BM homing and completely eradicates residual tumor in the BM. (A) Time schedule of in vivo functional evaluation of CXCR4GZMB-iNKs using THP-1-luciferase xenograft models. (B) Ex vivo bioluminescence imaging of femur to evaluate tumor burden of each group in the THP-1-luciferase xenograft models. After tumor inoculation, mice, untreated (n = 3), or treated with BFPGZMB-iNKs (n = 5) or CXCR4GZMB-iNKs (n = 5) were all euthanized at day 21 to obtain femurs. (C) Luminescence quantiﬁcation of ex vivo femur shown in panel D. (D) Residual THP-1 cells in BM analyzed by droplet digital PCR (ddPCR). (E) Distribution of iNKs in PB and BM (obtained from femur) detected at day 10 and 21, respectively. Technically, the cells extracted from BM were resuspended in the same volume of PBS between BFPGZMB-iNKs and CXCR4GZMB group. Left, Mann–Whitney U (D10) or unpaired t test (D21); right, unpaired t test with Welch’s correction. (F) Biodistributions of CXCR4GZMB-iNKs and BFPGZMB-iNKs in various tissues, including heart, liver, spleen, lung, kidney, BM, and PB. ‘Distribution index’ was determined as tissue-inﬁltrated iNKs detected by ddPCR and then normalized to the levels in PB. Values are presented as mean ± SD (C–F). Analyses of differences between groups were performed using Mann–Whitney U test (C,D,F). *P<0.05, **P<0.01; ns, no statistical signiﬁcance. Abbreviations: BM, bone marrow; CXCR4, C-X-C chemokine receptor type 4; GZMB, granzyme B; iNK, iPSC-derived natural killer cell; PB, peripheral blood.

Figure Legend Snippet: Figure 5. Regulatable CXCR4 in iPSC-derived NKs enhances BM homing and completely eradicates residual tumor in the BM. (A) Time schedule of in vivo functional evaluation of CXCR4GZMB-iNKs using THP-1-luciferase xenograft models. (B) Ex vivo bioluminescence imaging of femur to evaluate tumor burden of each group in the THP-1-luciferase xenograft models. After tumor inoculation, mice, untreated (n = 3), or treated with BFPGZMB-iNKs (n = 5) or CXCR4GZMB-iNKs (n = 5) were all euthanized at day 21 to obtain femurs. (C) Luminescence quantiﬁcation of ex vivo femur shown in panel D. (D) Residual THP-1 cells in BM analyzed by droplet digital PCR (ddPCR). (E) Distribution of iNKs in PB and BM (obtained from femur) detected at day 10 and 21, respectively. Technically, the cells extracted from BM were resuspended in the same volume of PBS between BFPGZMB-iNKs and CXCR4GZMB group. Left, Mann–Whitney U (D10) or unpaired t test (D21); right, unpaired t test with Welch’s correction. (F) Biodistributions of CXCR4GZMB-iNKs and BFPGZMB-iNKs in various tissues, including heart, liver, spleen, lung, kidney, BM, and PB. ‘Distribution index’ was determined as tissue-inﬁltrated iNKs detected by ddPCR and then normalized to the levels in PB. Values are presented as mean ± SD (C–F). Analyses of differences between groups were performed using Mann–Whitney U test (C,D,F). *P<0.05, **P<0.01; ns, no statistical signiﬁcance. Abbreviations: BM, bone marrow; CXCR4, C-X-C chemokine receptor type 4; GZMB, granzyme B; iNK, iPSC-derived natural killer cell; PB, peripheral blood.

Techniques Used: Derivative Assay, In Vivo, Functional Assay, Luciferase, Ex Vivo, Imaging, Digital PCR, MANN-WHITNEY

Figure 6. CXCR4+ CAR-iNKs demonstrate enhanced BM homing and anti-AML potency. (A) Time schedule of in vivo antitumor function evaluation of CXCR4+ CAR-iNKs using KG-1-luciferase xenograft models. (B) Tumor burden of each group in the KG-1-luc xenograft models monitored at the indicated time points. After tumor inoculation, mice were treated with CXCR4+ CAR-iNKs (n = 5) or CAR-iNKs (n = 5). (C) Statistical analysis of total bioluminescence of whole body (up) and bone marrow (bottom). Differences between groups were determined using two-way ANOVA. (D) Flow cytometry analysis of human NK cells (gated on ‘CD45+ CD56+ population’) and tumor cells (gated on ‘CD45+ CD56- population’) among tumor alone, CAR-iNKs, and CXCR4+ CAR-iNKs group. (E) Distribution of iNKs in PB and BM (obtained from femur) detected at day 21. Technically, the cells extracted from PB and BM were resuspended in the same volume between CXCR4+ CAR-iNKs and CAR-iNKs group. Left, unpaired t test with Welch’s correction; right, unpaired t test. (F) Biodistributions of CAR-iNKs and CXCR4+ CAR-iNKs in various tissues, including heart, liver, spleen, lung, kidney, and PB. Differences between groups were determined using Mann–Whitney U test or unpaired t test. Data are presented as mean ± SD (C,E,F). *P<0.05, **P<0.01, ****P<0.0001. Abbreviations: BM, bone marrow; CXCR4, C-X-C chemokine receptor type 4; GZMB, granzyme B; iNK, iPSC-derived natural killer cell; ns, no statistical signiﬁcance; PB, peripheral blood.

Figure Legend Snippet: Figure 6. CXCR4+ CAR-iNKs demonstrate enhanced BM homing and anti-AML potency. (A) Time schedule of in vivo antitumor function evaluation of CXCR4+ CAR-iNKs using KG-1-luciferase xenograft models. (B) Tumor burden of each group in the KG-1-luc xenograft models monitored at the indicated time points. After tumor inoculation, mice were treated with CXCR4+ CAR-iNKs (n = 5) or CAR-iNKs (n = 5). (C) Statistical analysis of total bioluminescence of whole body (up) and bone marrow (bottom). Differences between groups were determined using two-way ANOVA. (D) Flow cytometry analysis of human NK cells (gated on ‘CD45+ CD56+ population’) and tumor cells (gated on ‘CD45+ CD56- population’) among tumor alone, CAR-iNKs, and CXCR4+ CAR-iNKs group. (E) Distribution of iNKs in PB and BM (obtained from femur) detected at day 21. Technically, the cells extracted from PB and BM were resuspended in the same volume between CXCR4+ CAR-iNKs and CAR-iNKs group. Left, unpaired t test with Welch’s correction; right, unpaired t test. (F) Biodistributions of CAR-iNKs and CXCR4+ CAR-iNKs in various tissues, including heart, liver, spleen, lung, kidney, and PB. Differences between groups were determined using Mann–Whitney U test or unpaired t test. Data are presented as mean ± SD (C,E,F). *P<0.05, **P<0.01, ****P<0.0001. Abbreviations: BM, bone marrow; CXCR4, C-X-C chemokine receptor type 4; GZMB, granzyme B; iNK, iPSC-derived natural killer cell; ns, no statistical signiﬁcance; PB, peripheral blood.

Techniques Used: In Vivo, Luciferase, Flow Cytometry, MANN-WHITNEY, Derivative Assay

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Journal: Trends in biotechnology

Article Title: Regulatable C-X-C chemokine receptor type 4 in iPSC-derived NK cells improves bone marrow chemotaxis and targeting resident tumor.

doi: 10.1016/j.tibtech.2025.02.018

Figure Lengend Snippet: Figure 1. Limited bone marrow homing of IL15-iNKs could be rescued by overexpression of CXCR4. (A) RNA-seq reveals the transcriptional level of chemotaxis-associated genes in PBNKs, iNKs, and IL15-iNKs (n = 6 for each group). Statistical signiﬁcance was determined by one-way ANOVA or Kruskal-Wallis analysis, and Tukey test was used to analyze the speciﬁc difference group by group. (B) Flow cytometry analysis of CXCR4 expression on PBNKs, iNKs, and IL15- iNKs. (C) Experimental design to evaluate CXCR4 function in bone marrow (BM) homing using IL15-iNKs. IL15-iNKs were transduced with CXCR4 or luciferase (control), then infused into NOG mice for pharmacokinetic analysis (n = 5 for each group). Two groups of mice were euthanized to obtain BM from femur at day 7 (n = 2) and day 14 (n = 3). BM was resuspended by 200 μl phosphate buffered saline (PBS) for further analysis. (D) Pharmacokinetics of iNKs by detecting CD45+ CD56+ cells in the same volume of peripheral blood (left) and BM (right) at day 7 and day 14 using ﬂow cytometry. Statistical signiﬁcance was determined by unpaired t test. Data are presented as mean ± SD (D). *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001; ns, no statistical signiﬁcance. Abbreviations: CXCR4, C-X-C chemokine receptor type 4; iNK, iPSC-derived natural killer cell; PBNK, peripheral blood NK cell.

Article Snippet: To confirm correct transgene integration, genomic DNA was isolated from the iPSCs, followed by junction PCR and ddPCR analyse s. iNKs differentiation from engineered iPSC Human iPSC were cultured in StemFit Basic03 medium (Ajinomoto) supplemented with human bFGF on laminin-521 (LN-521)coated plates.

Techniques: Over Expression, RNA Sequencing, Chemotaxis Assay, Flow Cytometry, Expressing, Transduction, Luciferase, Control, Saline, Drug discovery, Cytometry, Derivative Assay

Journal: Trends in biotechnology

Article Title: Regulatable C-X-C chemokine receptor type 4 in iPSC-derived NK cells improves bone marrow chemotaxis and targeting resident tumor.

doi: 10.1016/j.tibtech.2025.02.018

Figure Lengend Snippet: Figure 2. Overexpression of CXCR4 affects hematopoietic differentiation of iPSC. (A) Diagram of engineering iPSC with varying levels of CXCR4 expression and their iNK differentiation. (B) Flow cytometry analysis of CXCR4 expression on edited iPSC. (C) Representative images of embryoid bodies (EBs) formed by different iPSC groups at day 9. (D) Flow cytometry analysis of hematopoietic stem and progenitor cell (HSPC) markers (CD43 and CD34) on cells isolated from EB. The gating strategy was built to exclude the isotype staining strictly. (E) Final iNK (CD56+ ) yields from CXCR4low iPSC clones (n = 3) and control iPSC clones (n = 2), demonstrated as ﬁnal iNKs from each starting iPSC cell. (F) Flow cytometry analysis of CXCR4 levels on iNKs of different groups. (G) Cytotoxicity analysis of CXCR4low iNKs and control iNKs by targeting GFP-labeled THP-1 tumor cells at a 3:1 Effector-to-Target (E:T) ratio in an IncuCyte-based functional assay. Data are presented as mean ± SD (D,E,G). Abbreviations: CXCR4, C-X-C chemokine receptor type 4; iNK, iPSC-derived natural killer cell.

Techniques: Over Expression, Expressing, Flow Cytometry, Isolation, Staining, Clone Assay, Control, Labeling, Functional Assay, Derivative Assay

Journal: Trends in biotechnology

Article Title: Regulatable C-X-C chemokine receptor type 4 in iPSC-derived NK cells improves bone marrow chemotaxis and targeting resident tumor.

doi: 10.1016/j.tibtech.2025.02.018

Figure Lengend Snippet: Figure 4. iPSC with targeted knock-in of CXCR4 at the GZMB locus demonstrate normal iNK differentiation and function. (A) Schematic view of targeted insertion of CXCR4 and BFP at GZMB locus. (B) Diagram illustrating the engineer process of CXCR4GZMB and BFPGZMB iPSC and their iNK differentiation process. (C) Representative images of EB formation of different groups of iPSC clones (upper panel). Flow cytometry analysis of hematopoietic stem and progenitor cell (HSPC)

Techniques: Knock-In, Clone Assay, Flow Cytometry

Journal: Trends in biotechnology

Article Title: Regulatable C-X-C chemokine receptor type 4 in iPSC-derived NK cells improves bone marrow chemotaxis and targeting resident tumor.

doi: 10.1016/j.tibtech.2025.02.018

Figure Lengend Snippet: Figure 5. Regulatable CXCR4 in iPSC-derived NKs enhances BM homing and completely eradicates residual tumor in the BM. (A) Time schedule of in vivo functional evaluation of CXCR4GZMB-iNKs using THP-1-luciferase xenograft models. (B) Ex vivo bioluminescence imaging of femur to evaluate tumor burden of each group in the THP-1-luciferase xenograft models. After tumor inoculation, mice, untreated (n = 3), or treated with BFPGZMB-iNKs (n = 5) or CXCR4GZMB-iNKs (n = 5) were all euthanized at day 21 to obtain femurs. (C) Luminescence quantiﬁcation of ex vivo femur shown in panel D. (D) Residual THP-1 cells in BM analyzed by droplet digital PCR (ddPCR). (E) Distribution of iNKs in PB and BM (obtained from femur) detected at day 10 and 21, respectively. Technically, the cells extracted from BM were resuspended in the same volume of PBS between BFPGZMB-iNKs and CXCR4GZMB group. Left, Mann–Whitney U (D10) or unpaired t test (D21); right, unpaired t test with Welch’s correction. (F) Biodistributions of CXCR4GZMB-iNKs and BFPGZMB-iNKs in various tissues, including heart, liver, spleen, lung, kidney, BM, and PB. ‘Distribution index’ was determined as tissue-inﬁltrated iNKs detected by ddPCR and then normalized to the levels in PB. Values are presented as mean ± SD (C–F). Analyses of differences between groups were performed using Mann–Whitney U test (C,D,F). *P<0.05, **P<0.01; ns, no statistical signiﬁcance. Abbreviations: BM, bone marrow; CXCR4, C-X-C chemokine receptor type 4; GZMB, granzyme B; iNK, iPSC-derived natural killer cell; PB, peripheral blood.

Techniques: Derivative Assay, In Vivo, Functional Assay, Luciferase, Ex Vivo, Imaging, Digital PCR, MANN-WHITNEY

Journal: Trends in biotechnology

Article Title: Regulatable C-X-C chemokine receptor type 4 in iPSC-derived NK cells improves bone marrow chemotaxis and targeting resident tumor.

doi: 10.1016/j.tibtech.2025.02.018

Figure Lengend Snippet: Figure 6. CXCR4+ CAR-iNKs demonstrate enhanced BM homing and anti-AML potency. (A) Time schedule of in vivo antitumor function evaluation of CXCR4+ CAR-iNKs using KG-1-luciferase xenograft models. (B) Tumor burden of each group in the KG-1-luc xenograft models monitored at the indicated time points. After tumor inoculation, mice were treated with CXCR4+ CAR-iNKs (n = 5) or CAR-iNKs (n = 5). (C) Statistical analysis of total bioluminescence of whole body (up) and bone marrow (bottom). Differences between groups were determined using two-way ANOVA. (D) Flow cytometry analysis of human NK cells (gated on ‘CD45+ CD56+ population’) and tumor cells (gated on ‘CD45+ CD56- population’) among tumor alone, CAR-iNKs, and CXCR4+ CAR-iNKs group. (E) Distribution of iNKs in PB and BM (obtained from femur) detected at day 21. Technically, the cells extracted from PB and BM were resuspended in the same volume between CXCR4+ CAR-iNKs and CAR-iNKs group. Left, unpaired t test with Welch’s correction; right, unpaired t test. (F) Biodistributions of CAR-iNKs and CXCR4+ CAR-iNKs in various tissues, including heart, liver, spleen, lung, kidney, and PB. Differences between groups were determined using Mann–Whitney U test or unpaired t test. Data are presented as mean ± SD (C,E,F). *P<0.05, **P<0.01, ****P<0.0001. Abbreviations: BM, bone marrow; CXCR4, C-X-C chemokine receptor type 4; GZMB, granzyme B; iNK, iPSC-derived natural killer cell; ns, no statistical signiﬁcance; PB, peripheral blood.

Techniques: In Vivo, Luciferase, Flow Cytometry, MANN-WHITNEY, Derivative Assay

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