CXCR4 dysfunction promotes HPV-associated chronic inflammation while preserving DC subset activation. (A) Representative images for hematoxylin and eosin coloration of flank skin sections (upper). Epidermal (arrowheads) thickness was measured along the tissue, with at least 10 measurements per sample (lower, mean ± SEM, n = 6-8 mice). Scale bar, 100 µm. (B) Representative confocal microscopy images (top) from epidermal sheets stained for CD207 (red). CD207⁺ cells were counted in 5 fields per sample (n = 3 samples per genotype) and the cell density calculated (bottom). Scale bars, 25 µm. (C) Percentage of cDC1, cDC2, and LCs among CD45⁺ skin cells. (D) Number of cDC1, cDC2, and LC per milligram of skin as the fold change relative to WT (see supplemental Figure 5 for the gating strategy, mean ± SEM, n = 9-11 per group, cumulative data from 4 independent experiments). (E) Representative histograms showing the surface expression of MHC2, CD80, and CD86 by cDC1, cDC2, and LCs from WT, +/1013, HPV, and HPV+/1013 mice. (F) Bar graphs show the expression of MHC2, CD80, and CD86 as the fold change relative to WT (mean ± SEM, n = 10-12 mice/group for MHC2 from 5 experiments, n = 9-11 mice/group for CD86 from 4 experiments, n = 7-9 mice/group for CD80 from 3 experiments). Mice had an FVB/N genetic background. Statistical analysis was performed using the 2-tailed, unpaired Mann-Whitney test to compare HPV mice and HPV+/1013 genotypes (A, **P < .01) or HPV and HPV+/1013 mice to their non-HPV counterparts (B-E, *P < .05, **P < .01, ***P < .005, ****P < .001).