pDC defects in Spi-B–deficient mice are cell intrinsic. A 1:1 mixture of CD45.2⁺ WT C57BL/6 or Spi-B–deficient BM cells with CD45.1⁺ WT BM cells were transferred to irradiated CD45.1⁺ WT C57BL/6 recipients. The resulting chimeric mice, WT + CD45.1→CD45.1 and Spib^−/− + CD45.1→CD45.1 mice, were analyzed 6-8 weeks after BM transfer. (A) BM pDCs, splenic pDCs, splenic cDCs, and splenic B cells were gated as CD19⁻CD11c⁺B220⁺, CD19⁻CD11c⁺B220⁺, CD19⁻CD11c⁺B220⁻, and CD19⁺CD11c⁻ cells, respectively. The percentages of CD45.2⁺CD45.1⁻ cells among these cells are shown. *P < .05; **P < .01. (B) CD45.2⁺CD45.1⁻ cells were gated and dot plots of CD11c versus BST2 in BM, spleen, and iLN cells are shown. Numbers indicate percentages of gated cells among CD45.2⁺CD45.1⁻ cells. For PB cells, dot plots of CD11c versus BST2 in CD19⁻CD11c⁺B220⁺ cells are shown. Numbers indicate the percentages of gated cells among CD45.2⁺CD45.1⁻CD19⁻CD11c⁺B220⁺ cells. (C) CD45.2⁺CD45.1⁻CD19⁻CD11c⁺B220⁺ cells were gated and analyzed for the expression of Ly49Q. Open histograms indicate isotype controls. Numbers indicate percentages and mean fluorescence intensity of Ly49Q⁺ cells. Experiments were performed 2 times using 6 WT + CD45.1→CD45.1 and 7 Spib^−/− + CD45.1→CD45.1 mice in total. Panel A shows the data from one experiment; panels B and C show representative data.