PS exposure by B cells is strain dependent. (A) Lymphocytes from NZW and DBA/2 mice were labeled with anti-CD19^APC and anti-CD19^PERCP antibodies, respectively (to allow B cells from each strain to be easily distinguished), mixed, and preincubated with AV^FITC. Panels show density plots of the rate of PS exposure (binding of AV) by B cells from NZW (left panel) and from DBA/2 mice (center panel) measured in the same tube following stimulation with 3 μM calcimycin (arrows). The right panel shows an alternative representation of the same data, plotted as the percentage of cells with exposed PS as a function of time. (B) An equivalent experiment to that in panel A but with lymphocytes derived from NOD and C57BL/10 mice. (C) Cells were stained as in panel A to identify B-cell populations after mixing. Bars show the percentage (mean ± SD, n = 4) of B cells from DBA/2 and NZW (left panel), or NOD and C57BL/10 mice (right panel), with exposed PS approximately 7 minutes after stimulation with 3 μM calcimycin. (D) Cells from NZW and NOD mice were stained as in panel A to distinguish B-cell populations. Panels show density plots of the rate of PS exposure (binding of AV) by B cells from NZW (left panel) and NOD mice (center panel) following stimulation with 3 μM calcimycin (arrows). The rate of PS exposure was equivalent in the 2 strains. In similar experiments, the rate of PS exposure by B-cell populations from NOD and/or NZW mice was faster than that that by cells from 129, C3H, CBA, FVB/n, and NIH mice (not shown).