BCL-2 facilitates NK and T cell–mediated killing. (A) CFSE-based proliferation assay of Eμ-myc/p53^+/− (± BCL-2) and Eμ-myc/vav-bcl-2 (± dnp53) cells. Eμ-myc/p53^+/− (± BCL-2, n = 2 each) and Eμ-myc/vav-bcl-2 (± dnp53, n = 3 each) cell lines were subjected to FACS analysis, no difference in proliferation was detected (values represent mean MFI ± SD). 7-AAD⁺ dead cells were excluded; no differences between the different groups in 7-ADD⁺ cells were evident. (B) Transplantation of indicated cell lines into Rag2^−/−cγ^−/− mice. No statistically significant difference in survival time between the groups analyzed could be detected (Eμ-myc/p53^+/−, n = 8; Eμ-myc/p53^+/− + BCL-2, n = 8; P = .2). (C) FACS analysis of H2-D^b (MHC class I), MULT1, and RAE1 in Eμ-myc/p53^+/− (n = 4) and Eμ-myc/vav-bcl-2 (n = 3) cell lines. Eμ-myc/p53^+/− cells expressed significantly less MULT1 than with Eμ-myc/vav-bcl-2 cells (P = .0494) and lower levels of RAE1 (P = .1356). (D) NK-cell cytotoxicity assay with the use of different Eμ-myc tumor cell lines as targets as indicated in the figure. Purified and in vitro–expanded NK cells were incubated at different E:T with CFSE-labeled Eμ-myc cells for 4 hours. The percentage of NK cell–specific tumor cell lysis is depicted. (E) T cell–mediated lysis of Eμ-myc tumor cells. CD8⁺ effectors were coincubated with CFSE-labeled tumor target cells for 20 hours in ascending E:Ts, which were calculated after FACS-based quantification of CD8⁺ cytotoxic T cells within the effector cell suspensions. The percentage of T cell–specific tumor cell lysis is depicted.