Loss of MHC-I-immunosurveillance in NKCKD mice is because of silencing of Ly49 that bind to self–MHC-I. Three different Ly49-transgenes were introduced into NKCKD mice by breeding. (A-C) Flow cytometric analysis of Ly49 expression in Ly49tg-NKCKD NK cells. Ly49 staining of NK cells is shown for (A) NKCKD-Ly49Atg, (B) NKCKD-Ly49Gtg, and (C) NKCKD-Ly49Itg mice as a black histogram. The gray histogram shows control staining of splenic NK cells from NKCKDmice. (D-F) Specific rejection of B2m−/− splenocytes by (D) Ly49Atg-NKCKD mice, (E) Ly49Gtg-NKCKD mice, (F) Ly49Itg-NKCKD mice in comparison to WT or NKCKD mice. Each symbol represents the data from a single mouse. Data are pooled from 3 to 5 independent experiments. Groups differed significantly as shown (*P < .05; ***P < .001; NS indicates not significant). (G) LAK prepared from WT, NKCKD, and NKCKD-Ly49itg mice were used as effector cells in a 51Cr-release assay against B2m−/− ConA blasts. These experiments were performed with mice on the B6 background.