CXCR4 controls steady-state skin DC migration and in acute inflammation. (A) Representative dot plots showing migDCs (CD11c⁺MHC2^hi gated on CD3⁻CD19⁻CD317⁻) in inguinal LNs from WT, +/1013, HPV, and HPV+/1013 mice. Percentages among parent cells are indicated. (B-C) Percentage among singlets (B) and number (C) of migDCs per LN as the fold change relative to WT values. (B-C) Mean ± SEM, n = 10-11 per group, cumulative data from four independent experiments. (D) Representative dot plots showing the gating strategy for identifying CD103⁺ migDC1 and CD103⁻ migDC2+LC subsets in SDLNs from mice 24 hours after FITC treatment. (E) Number of FITC-negative (FITC⁻) and FITC-positive (FITC⁺) migDCs in skin-draining LNs from FITC-treated mice. (F) Membrane expression of CCR7 (left) and CXCR4 (right) by FITC⁺ migDC1 and migDC2+LC from WT and +/1013 mice. (G) Left, experimental design: mice received AMD3100 or PBS at t = 0 and 6 hours. FITC was applied at t = 1 hour. Right, number of FITC⁺ migDC1 and migDC2+LC in inguinal LNs form mice treated or not with AMD3100 (AMD). Mean ± SEM, n = 8-9 mice/group, cumulative data from 2 independent experiments (D-F). Mean ± SEM, n = 6-8 mice/group, cumulative data from 3 independent experiments (G). Mice had an FVB/N genetic background. Statistical analysis was performed using the 2-tailed, unpaired Mann-Whitney test to compare WT and +/1013 mice. *P < .05, **P < .01.