NKR-P1B-deficient mice show impaired acute rejection of Clr-b-deficient splenocytes but enhanced rejection of MHC-I-deficient splenocytes. (A) Rejection of 5-(and 6)-carboxyfluorescein diacetate succinimidyl ester (CFSE)-labeled splenocytes from Clr-b^−/− mice 18 hours after injection. Some mice were treated with poly(I:C) or CpG-B ODN for 24 or 6 hours, respectively, before CFSE-labeled splenocyte injection. Each symbol represents an individual mouse. Small horizontal bars represent mean values. Data are pooled from multiple experiments. (B) Rejection of CFSE-labeled splenocytes from Clr-b^−/− mice 18 hours after injection. Some of the WT mice were treated with anti-NKR-P1C antibody (NK1.1) to deplete NK cells (NK-depleted). All mice were treated with CpG-B ODN for 6 hours before CFSE-labeled splenocyte injection. Each symbol represents an individual mouse. Small horizontal bars represent mean values. Data are pooled from 2 independent experiments. (C) Rejection of CFSE-labeled splenocytes from B2m^−/− and B2m^−/−Clr-b^−/− mice at different time points after injection. Mice were not stimulated before splenocyte injection. Mean ± SD of percent rejection at each time point is shown. Data are pooled from multiple experiments. Statistical analysis was performed by Student t test, and P values are indicated. (D) Ability of LAK cells from WT and NKR-P1B-deficient mice to mediate cytotoxicity toward B2m^−/− or B2m^−/−Clr-b^−/− BM-DCs was tested by ⁵¹Cr-release assay. Data are represented as the mean ± SD of percent killing measured in triplicate. Statistical analysis was performed by Student t test, and P values are indicated.