Figure 4.
CD3ζ-disuption does not impede canonical NK cell functions in vitro. (A) CD3ζ editing outcomes assessed by flow cytometry. (B) Cytotoxicity of primary CD3ζ disrupted NK cells in simple 16 hours coculture assay with K562 cells, Nalm-6 cells or allogeneic PBMC (n = 3 biological replicates). (C) Degranulation of primary CD3ζ disrupted NK cells assessed by flow cytometry (n = 3 biological replicates; two-way ANOVA followed by Dunnett’s multiple comparison test with a single pooled variance). (D) Expression of CD16 and CD3ζ in wild-type NK-92 cells and primary NK cells after CD3ζ-disruption. (E) ADCC of primary CD3ζ-disrupted NK cells against CD20+ bGal− Jeko-1 cells at different concentrations of antibodies specific for CD20 (rituximab) or bGal (n = 3 biological replicates, each in 3 technical replicates).

CD3ζ-disuption does not impede canonical NK cell functions in vitro. (A) CD3ζ editing outcomes assessed by flow cytometry. (B) Cytotoxicity of primary CD3ζ disrupted NK cells in simple 16 hours coculture assay with K562 cells, Nalm-6 cells or allogeneic PBMC (n = 3 biological replicates). (C) Degranulation of primary CD3ζ disrupted NK cells assessed by flow cytometry (n = 3 biological replicates; two-way ANOVA followed by Dunnett’s multiple comparison test with a single pooled variance). (D) Expression of CD16 and CD3ζ in wild-type NK-92 cells and primary NK cells after CD3ζ-disruption. (E) ADCC of primary CD3ζ-disrupted NK cells against CD20+ bGal Jeko-1 cells at different concentrations of antibodies specific for CD20 (rituximab) or bGal (n = 3 biological replicates, each in 3 technical replicates).

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