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. 2015 Aug 28;5(4):597–608. doi: 10.1016/j.stemcr.2015.07.011

Figure 5.

Figure 5

Induction of Apoptosis in iC9-iPSC-Derived CTLs by Activation of iC9

(A) Flow cytometric analysis of annexin V binding and 7-AAD uptake by rejT-NT-HIV1 and rejT-iC9-HIV1 24 hr after CID treatment (left). Original EBV-CTLs, rejT-NT-EBV, rejT-iC9-EBV, rejT-NT-HIV1, and rejT-iC9-HIV1 were left untreated or treated with CID. Apoptosis was assessed 24 hr after treatment. Data are representative of three independent triplicate experiments. Error bars represent ± SD. ∗∗∗∗p < 0.0001 by two-way ANOVA.

(B) In vivo bioluminescent imaging of rejT-iC9-EBV expressing FFluc. NOD-Scid mice inoculated intraperitoneally with EBV-LCL cells and with rejT-iC9-EBV cells received three doses of CID (50 μg) intraperitoneally (n = 4). Comparison mice received no CID (n = 3). Images of three representative mice from each group are shown.

(C) FFluc signal intensities after rejT-iC9-EBV cell transfer in each group. Error bars represent ± SEM. p < 0.05 by unpaired Student’s t test (two-tailed).

(D) Study schema of in vivo rejT-iC9-mCherry detection in peripheral blood (upper). mCherry expression was quantified by flow cytometry (n = 4 per group). Representative data of three experiments are shown (lower).

(E) Schematic illustration of the iC9/CID safeguard system to protect patients receiving iPSC-derived CTL therapy.

See also Figure S3.