Skip to main content
. Author manuscript; available in PMC: 2018 Feb 16.
Published in final edited form as: J Immunol. 2010 Mar 15;184(8):4247–4257. doi: 10.4049/jimmunol.0902914

Figure 7. Depletion of CD11chiMHCIImed cells in CD11c-DTR bone marrow chimeras disrupts vascular quiescence and stabilization.

Figure 7

Wild-type mice reconstituted with CD11c-DTR bone marrow received footpad injection of BMDCs on day 0 and 200ng DT or CRM intraperitoneally on day 6. Popliteal nodes were harvested at day 7. CD11c+ cell subsets were gated as in Figs. 2A and 3A. (A) CD11chiMHCIImed cell numbers. (B) Ratio of CD11chiMHCIImed (R1) cells to CD11cmed (R2+R3) cells. (C) Proliferation of total CD45−CD31+ endothelial cell population. (D) Proliferation of PNAd+ endothelial cells. (E) Relative HEV trafficking efficiency. Values in DT-treated mice were normalized to that of the CRM-treated controls in each experiment. (F) VCAM-1 expression level on PNAd+ endothelial cells. For (A–F), n = 4–8 mice per group. (G) Vascular permeability as indicated by Evans blue content in lymph nodes. n=4 mice per group. (H) Percent of T zone HEV that have disrupted FRC organization. Results represent at least 24 fields over 5 lymph nodes for each condition. For (A–H), *=p<0.05; **= p < 0.01 with the Student’s t test.