(A) B6 splenocytes were transduced with the retroviral vector TRP-2–CSM encoding TRP-2 and the ΔLNGFr marker. (B) Transduction efficiency. Ninety percent of CD3⁺ cells (middle and right panels) expressed ΔLNGFr (right panel). Mock-transduced splenocytes were negative (middle panel). (C) B6 mice were treated with mock-transduced GMLs; TRP-2–GMLs from WT (TRP-2 WT) or β2m^–/– mice (TRP-2 β2m^–/–); or DCs pulsed with 2 TRP-2 peptides (TRP-2–pulsed DCs). TRP-2–GMLs from both WT and β2m^–/– mice were able to control tumor growth. *P = 0.03, **P < 0.05; Student’s t test. (D) The infusion of TRP-2–GMLs elicits TRP-2–specific cytotoxic T cells. Splenocytes from vaccinated mice were restimulated in vitro with TRP-2 peptides and tested in a cytotoxicity assay against pulsed (filled symbols) or unpulsed (open symbols) RMA cells. (E) Induction of memory antitumor responses. Forty days after vaccination, B16 cells were implanted s.c. TRP-2–GMLs from both WT and β2m^–/– mice were able to control tumor growth. ^†P < 0.005,^‡P < 0.0005; Student’s t test. Data shown in C and E are representative of 2 experiments with 5 mice/group. (F) Kaplan-Meier survival graphs. Mice were treated as described in Methods. Statistical comparison of the survival curves, performed by the log-rank test, gave the following results: 4 × 10⁶ TRP-2–GMLs versus mock-GMLs, P < 0.005; 10 × 10⁶ TRP-2–GMLs versus mock-GMLs, P < 0.005; TRP-2–pulsed DCs versus mock-GMLs, P < 0.005.