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. 2003 Sep 1;198(5):757–769. doi: 10.1084/jem.20030794

Figure 2.

Figure 2.

The defect causing abnormal differentiation of MECs in LTβR−/− and aly/aly mice lies in the stroma compartment. (A) Thymus sections of the indicated bone marrow chimeras were analyzed 6–8 wk after bone marrow transfer. The middle and right panels in the top row represent consecutive sections to demonstrate the presence of wild-type thymocytes. The staining reagent is indicated in parentheses. The left panels in the top and the bottom row are low magnification images of the subsequent panels. (B) UEA-1–positive MECs in LTβR−/− and wild-type mice were counted on 10 high power fields for each genotype. (C) MECs in preparations of thymic epithelial cells of single thymi from LTβR−/− and wild-type mice were identified and counted by FACS® analysis. The overall size of LTβR−/− thymi as measured by thymocyte numbers did not significantly differ from control thymi (see Fig. 6). Histogram plots are electronically gated on cells negative for CD45 and CDR1, and the marker indicates the fluorescence intensity scored as high level UEA-1 expression. MEC numbers of four individual thymi per genotype were determined. (D) The absolute number of CD45−G8.8+CDR1−B7.1+ MECs from preparations of epithelial cells of pools from five mice were determined. The gate that identifies these MECs among CD45−G8.8+ thymic epithelial cells is shown in Fig. 7. The results of three independent experiments for each genotype are shown. Error bars represent standard deviations from the mean and statistical analysis was done using Student's t test.