Induction of CTL responses by peptide-pulsed DCs is impaired by addition of imatinib mesylate. Mobilized human CD34⁺ PBPCs were cultured in the presence of GM-CSF, TNF-α, IL-4, and FLT3L with or without imatinib mesylate (3 μM) and used for the induction of primary Her-2/neu–specific CTL (A-B) or to elicit a CTL response against a recall antigen (IMP; C-D). (A) DCs were pulsed with the synthetic HLA-A2–binding peptide E75 derived from Her-2/neu tumor-associated antigen and used as APCs to induce a CTL response. The cytotoxic activity was determined after 2 restimulations in a standard ⁵¹Cr-release assay using Croft cells (HLA-A2⁺, Her-2/neu^–) pulsed with E75 (▪) or HIV peptide (□), SK-OV-3 cells (HLA-A3⁺, Her-2/neu^–; ▴), K 562 cells (♦) and A498 cells (HLA-A2⁺, Her-2/neu⁺) with (○) or without (•) blocking HLA-A2 antibody as target cells. (B) DCs generated with 3 μM imatinib mesylate were used as APCs in the setting described in panel A. (C) DCs were pulsed with the IMP peptide and used as APCs for CTL induction. The cytotoxic activity was determined after 2 restimulations in a standard ⁵¹Cr-release assay using Croft cells pulsed with IMP peptide (▪) or HIV peptide (□) and K 562 cells (♦). (D) DCs generated with 3 μM imatinib mesylate were used as APCs in the setting described in panel C. E/T indicates effector-target ratio.