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. 2019 Sep 7;8(11):1659095. doi: 10.1080/2162402X.2019.1659095

Figure 4.

Figure 4.

Killing capability of PSMA PLT-TM redirected UniCAR T cells. (a–d) In order to compare the killing capability of UniCAR T cells (UniCAR 28/ζ) armed with either the PSMA PLT-TM or the αPSMA scFv-TM, chromium release assays were performed using either PSMA-positive (a, c) LNCaP or (b, d) PC3 tumor cells. (a, b) As negative controls served UniCAR T cells transduced with an EGFP-expressing vector control (vector control) or UniCAR construct lacking the signaling domains (UniCAR Stop). Data are reported as mean ± SEM for three independent donors. (***p < .0002, **p < .002, *p < .033 with respect to UniCAR 28/ζ w/o TM; 2way ANOVA with Tukey’s multiple comparisons test). (c, d) In order to estimate the range of working concentration for the PSMA PLT-TM PSMA-positive (c) LNCaP cells or (d) PC3 cells were co-cultivated with human T cells modified with the UniCAR signaling construct at an E:T ratio of 5:1. The TM was added at indicated concentrations. Specific lysis of tumor cells was estimated by chromium release assays (see Materials and methods). Data are reported as mean ± SEM for indicated number of independent donors. (***p < .0002, **p < .002 with respect to UniCAR 28/ζ w/o TM; 2way ANOVA with Sidak’s multiple comparisons test). (e) PSMA-positive PC3 cells were incubated with UniCAR T cells in the presence (w/TM) or absence (w/o TM) of the PSMA PLT-TM. Images were taken at the start (10 min), after 60 min, 120 min, 180 min, and 210 min.