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. 2022 Jun 13;119(25):e2122379119. doi: 10.1073/pnas.2122379119

Fig. 6.

Fig. 6.

scRNA-seq analyses reveal crosstalk between CAR-mb15 CIML NK cells and AML target cells. (A) tSNE clustering analysis of CAR+ NK cells cocultured with or without AML target cells. CIML NK cells generated from two PB donors were transduced with NPM1c-CAR-mb15 lentivirus, and purified viable NK cells were cocultured with OCI-AML3 cells for 24 h followed by scRNA-seq. (B) Cell proportion of identified clusters in CAR+ NK cells cocultured with or without AML target cells; cluster 2 was consistently increased in CAR+ NK cells cocultured with AML targets. (C) Volcano plot of gene expression between cluster 2 and other clusters. Blue dots: down-regulated; and orange dots: up-regulated DEGs. (D) Dot plots of the expression of selected genes. (E) GO functional enrichment analysis of DEGs in C. (F) Fold-change of IFNγ, CD107a, perforin, and granzyme B in NPM1c-CAR-mb15 CIML NK cells over untransduced (Ctrl) CIML NK cells. CIML NK cells from three different donors were cocultured with OCI-AML3 target cells for 5 h followed by mass cytometry analysis. (G) The scores for maturation, cytotoxicity, KIR, and inhibition in each cluster. (H) Comparison of selected marker expression by NPM1c-CAR-mb15 CIML NK cells and the untransduced CIML NK cells from the same donor. CAR+ and CAR− CIML NK cells were cocultured with AML target cells for 5 h and analyzed by mass cytometry. The heatmap shows median values in protein expression levels of the indicated activation markers and receptors. n = 2 (A–E and G) and 3 (F) PB donors. Data are representative of two (H) independent experiments or pooled from two (F) independent experiments.