The therapeutic CTCL model was further extended to evaluate the role of human effector cells in tumor cell killing using bioluminescence imaging (BLI) of luciferase expressing CCR4 + Mac-1 cells established by retroviral transduction. Ten SCID-BEIGE mice that were grafted with 1610 6 CCR4 + Mac-1 cells and developed equivalent sized tumors as detected on day 7 by BLI were divided into two groups. Eleven days after initial tumor cell inoculation, the AAV8-minibody vectors were administered intravenously. Next, human PBMCs (hPBMCs) were given by intraperitoneal injection 7 days after AAV vector administration. As shown in Figure 3a , treatment with AAV8-h1567 and hPBMCs resulted in substantial tumor growth inhibition compared to AAV8-11A plus hPBMC treated mice. Quantitative monitoring of tumor growth by in vivo BLI correlated with visible tumor growth, further confirming the tumor growth inhibition effect of AAV8-h1567 compared with control group (Figure 3b) . A significant difference was observed between the control AAV8-11A and therapeutic AAV8-h1567 groups on days 40, 42, and 45 after tumor inoculation by caliper measurement and by days 25 and 38 by BLI (Figure 3a and b) . Real-time whole-body BLI of a representative mouse showed that tumor growth was considerably inhibited in mice treated with AAV8-h1567 compared with control mice over the treatment period ( Figure 3c) . Analysis of micro-computed tomography/positron emission tomography (mCT/PET) images also revealed tumor growth inhibition with AAV8-h1567 treatment compared with the control group. While both AAV8-h1567 and AAV8-11A showed primary tumor growth 28 days after tumor inoculation, the tumor cells became much more locally invasive in the AAV8-11A treated group and showed increased metabolic activity as indicated by the accumulation of the PET tracer 18 F-fluorodeoxyglucose (FDG) in whole-body images of mice (Figure 3d) .