Activation of the iCasp-9 suicide gene eliminates the IL-2 and IL-15 transgenic CTLs in vivo. SCID mice engrafted subcutaneously with LCLs were injected intravenously with EBV-CTLs transduced with either iC.ΔCD34/IL-2v or iC.ΔCD34/IL-15v vector, sorted for ΔCD34 expression, and transduced with eGFP-FFLuc vector. When the CTLs were expanding, mice were treated with 2 to 3 doses of the CID AP20187 (50 μg) intraperitoneally 2 days apart. The persistence of the transgenic cells was monitored in vivo using the bioluminescence system. Panel A illustrates in a representative experiment the reduction of the bioluminescence after CID administration. Bioluminescence was significantly reduced in mice receiving IL-2 or IL-15 transgenic CTLs after treatment with CID. In contrast, the signal was not diminished in mice receiving control ΔCD34⁺ CTLs lacking the expression of the suicide gene. The bioluminescence continued to increase in mice receiving IL-15 transgenic CTLs nontreated with CID. Panel B shows the kinetics of bioluminescence in 7 mice (closed symbols) before and after treatment with CID. In mice receiving EBV-CTLs expressing either iC.ΔCD34/IL-2v or iC.ΔCD34/IL-15v followed by the CID greater than 1 log reduction in bioluminescence was observed. In contrast, bioluminescence continued to increase in mice nontreated with CID (4 representative mice, open symbols). (C) Mice showing > 10⁶ photons were euthanized to evaluate the infiltrate of CTLs within the tumor by FACS analysis after staining with antihuman CD3 antibody (top left panel). Mice with similar level of bioluminescence signal were treated with CID and 24 to 72 hours later euthanized to evaluate the effective reduction of CTL infiltration by FACS analysis after staining with antihuman CD3 antibody (top right panel). CID did not reduce the number of CD3⁺ cells in mice receiving control CTLs transduced with ΔCD34v vector (bottom left and right).