Transduction with CN mutants allows EBV-CTL proliferation in the presence of CN inhibitors. EBV-CTLs were transduced with either a CN mutant or with GFP control after stimulation 2. CN inhibitors were added at stimulation 4, and CTL growth was assessed for 3 weeks (mean and SEM shown, n = 5). (A) In the absence of CN inhibitors, growth of transduced CTLs and untransduced CTLs is comparable over 3 weeks (P = .675). (B) Expansion of EBV-CTLs over time with or without FK506/CsA. (Bi) Untransduced CTLs are suppressed by either FK506 or by CsA. (Bii) GFP-transduced CTLs are suppressed by either CN inhibitor. (Biii) CNa12-transduced CTLs proliferate in the presence of FK506 but not CsA. (Biv) CNa22-transduced CTLs proliferate in the presence of CsA but not FK506. (Bv) CNb30-transduced CTLs proliferate in the presence of either FK506 or CsA. (C) ³H-thymidine uptake assay after stimulation with autologous LCLs in the presence or absence of CN inhibitors. CNa12 confers 90% resistance to FK506, CNa22 confers 103% resistance to CsA, and CNb30 confers both 83% resistance to FK506 and 86% resistance to CsA (median and interquartile range shown, n = 5).