Figure 3.
Venetoclax treatment increases NK cell avidity for AML cells and promotes lytic granule polarization during immune synapse formation
(A) Volcano plot of differentially expressed genes (DEGs) between the control and venetoclax-treated groups, with selected DEGs labeled.
(B) The distribution of DEG values in each sample from RNA-seq while classifying genes with similar functions.
(C) GO term enrichment analysis of upregulated DEGs in the venetoclax-treated group.
(D) F-actin (red) and perforin (green) staining in cell conjugates was acquired at different time points after mixing CB-NK cells (1 × 105 cells per well) treated or untreated with 400 nM venetoclax with KG-1a cells at a ratio of 1:1.
(E) Granule-to-synapse distance was quantified for 15–55 conjugates per group. The results represent two independent experiments.
(F) Schematic diagram of the single-cell avidity binding experimental outline.
(G) Representative bright-field raw micrographs of a microfluidic chip loaded with KG-1a cells and exposed to venetoclax-treated or untreated NK cells for 10 min before gradually applying force up to 1,000 pN. Orange circles represent bound effectors, while green circles represent regions where effectors were bound at the start of force application but then dislodged.
(H) Evaluation of binding avidity between venetoclax-treated or untreated NK cells and KG-1a targets using acoustic force microfluidic microscopy.
(I) Normalized fold change in the binding of venetoclax-treated NK cells compared to that of untreated NK cells from (H), n = 3.
(J) Cell-binding avidity from (H) at 1,000 pN, n = 3.
Data are presented as mean ± SD for (H)–(J). Statistical significance was determined using unpaired Student’s t test (E and J).
See also Figure S3.