Natural killer gene complex knockdown (NKC^KD) NK cells exhibit defective in vitro killing of MHC-I–deficient ConA blasts, and NKC^KD mice exhibit reduced rejection of MHC-I–deficient splenocytes in vivo. The ability of lymphokine-activated killer (LAK) cells from WT and NKC^KD to kill splenic ConA blast target cells from (A) B6 (WT), (B) B2m^−/−, (C) H2K^b−/−H2D^b−/−, (D) H2K^b−/−, (E) H2D^b−/−, and (F) Rae-1ϵ transgenic (Rae-1ϵ^tg) mice was tested by ⁵¹Cr-release assay. Data are represented as the mean ± SD percentage of chromium release from triplicate wells. Data are representative of 3 similar experiments. Cytotoxicity experiments were performed with mice on the B6 background. (G) The ability of WT and NKC^KD mice to reject CFSE-labeled splenocytes from B2m^−/−, H2K^b−/−H2D^b−/−, H2K^b−/−, and H2D^b−/− mice was tested by flow cytometry of recipient splenocytes 16 hours after injection. Each symbol represents the data from an individual mouse, and the small horizontal lines indicate the mean. Some mice of each strain were pretreated with anti–asialo-GM1 Ab to deplete NK cells before injection of CFSE-labeled cells. Data are pooled from 3 to 5 independent experiments. Groups differed significantly as shown (***P < .001; NS, not significant). (H) Time-course rejection assay of B2m^−/− splenocytes by WT and NKC^KD mice. Data are displayed as the mean ± SEM rejection of 6 individual mice. Splenocyte rejection experiments were performed with 129S1 background mice.