Figure 3. Depletion of CD11c^hiMHCII^med cells disrupts endothelial cell quiescence.

(A–I) Wild-type (WT) or CD11c-DTR (DTR) mice were injected with BMDCs on day 0 and received intraperitoneal injection of 100ng DT or CRM on day 6. Popliteal nodes were harvested at day 7. (A) Flow cytometry plot showing effect on CD11c+ subsets with DT treatment of DTR mice. (B) Number of cells in each CD11c+ subset. (C)Ratio of CD11c^hiMHCII^med (R1) cell numbers to CD11c^med (R2+R3) cell numbers. (D) Proliferation of total CD45−CD31+ endothelial cell population. (E) Proliferation of CD45−CD31+PNAd+ HEV endothelial cells. (F) Proliferation of CD45−CD31+PNAd− endothelial cells. (G) HEV trafficking efficiency. (H) VCAM-1 expression level on PNAd+ endothelial cells. (I) Total cell number per lymph node. For (B–I), n ≥ 6 mice for each condition. *=p<0.05; **= p < 0.01; ***= p < 0.001 with the Student’s t test. (J–K) Unstimulated CD11c-DTR mice received DT or CRM at day 0 and were examined at day 2. (J) Number of cells in each CD11c+ subset. (K) Proliferation of CD45−CD31+ endothelial cells. For (J–K), n ≥ 4 mice for each condition. *=p<0.05. For (J), asterik refers to comparison with the same CD11c+ subset in CRM-treated mice.