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. 2024 Feb 27;12(2):e008155. doi: 10.1136/jitc-2023-008155

Figure 2.

Figure 2

Downregulation of ICAM-1 results in escape from trastuzumab-mediated ADCC. (A) Flow cytometric analysis of ICAM-1, ICAM-2, and ICAM-3 expression on MDA-MB-453 cells. Filled gray areas indicate isotype controls. (B) ICAM-1 and ErbB2 expression on K562 and MDA-MB-453 ICAM-1 knock-out (KO) cells, and non-targeting sgRNA transduced (NT) or parental wild type (WT) control cells. Representative data from at least three independent experiments are shown. (C, D) haNK cells combined with trastuzumab (C) or NK-92 (D) cells were co-cultured for 2 hours with MDA-MB-453 or K562 ICAM-1 KO or NT and parental WT control cells at an effector to target ratio of 10:1 as indicated. Specific cytotoxicity was measured using a Europium-based cytotoxicity assay. Values for ICAM-1 KO and NT control cells are plotted relative to those obtained with parental WT MDA-MB-453 or K562 cells. To confirm trastuzumab-mediated ADCC against MDA-MB-453 cells, control samples without trastuzumab were included. Data were pooled from at least three independent experiments. Mean values±SEM are shown. ADCC, antibody-dependent cell-mediated cytotoxicity; haNK, high-affinity FcγRIIIa-modified natural killer-92 cells.