CXCR4 dysfunction promotes steady-state DC activation and in the context of HPV-associated inflammation. (A) Representative histograms showing the levels of MHC2, CD80, and CD86 surface expression by migDCs and resDCs (defined as CD11c⁺MHC2^hi and CD11c^hiMHC2⁺ gated on live CD3⁻CD19⁻CD317⁻ cells, respectively) recovered from the SDLNs of WT, +/1013, HPV, and HPV+/1013 mice. (B) Bar graphs showing the surface expression of MHC2, CD80, and CD86 for migDCs and resDCs as the fold change relative to WT. (C) Bar graphs showing the expression of MHC2 and CD86 in pDCs as the fold change relative to WT. Mean ± SEM, n = 8-11 mice/group from 4 experiments for MHC2, n = 8 mice/group from 3 experiments for CD86, n = 6 mice/group from 2 experiments for CD80 (B-C). (D) Bar graphs showing the surface expression of MHC2, CD86, and CCR7 for migDC1 and migDC2+LC from HPV and HPV+/1013 mice (mean ± SEM, n = 6-7 per group from 1 of 2 representative experiments). (E) Bar graphs showing the surface expression of MHC2 and CD86 upon LPS or ssRNA stimulation for DC1-like and DC2-like BMDCs derived from WT and +/1013 mice. Results are expressed as the fold change relative to nontreated WT (mean ± SEM, cumulative data from n = 4 to 5 independent experiments). Mice had an FVB/N genetic background. Statistical analysis was performed using the 2-tailed, unpaired Mann-Whitney test to compare +/1013 mice to their WT counterparts. **P < .01, ***P < .005.