Supplementary Figure S2 from Development of Engineered T Cells Expressing a Chimeric CD16-CD3ζ Receptor to Improve the Clinical Efficacy of Mogamulizumab Therapy Against Adult T-Cell Leukemia

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ADCC activity mediated by cCD16ζ-T cells against Mog-opsonized ATL tumor cells was dependent on both effector cell number and Mog dose. However, at a pharmacological dose of Mog, the decline of ADCC was more obviously dependent on the number of effector cells. (a) At a pharmacological dose of Mog (1μg/mL), ADCC activity mediated by cCD16ζ-T cells against Mog-opsonized ATL tumor cells declined sharply when the number of effector cells was lower. In order to exclude NK cell activity, K562-A24 was employed in this experiment as a negative control. Each experiment at the indicated dose of Mog was conducted in triplicate using three independent sets of cells from three different healthy donors. LCL, EBV-immortalized B cell line; Mog, mogamulizumab. Each experiment was conducted in triplicate (n=3). Error bars depict SD. (b) In the presence of a sufficient number of effector cells (E/T ratio 5:1), ADCC activity mediated by cCD16ζ-T cells against ATL tumor cells was also Mog dose-dependent. However, at pharmacological doses of Mog (>0.1μg/mL), the decline of ADCC activity was limited in comparison to that observed in S2a. LCL, EBV-immortalized B cell line: Mog, mogamulizumab. Each experiment was conducted in triplicate (n=3). Error bars depict SD.

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