CD11c-specific depletion of p14 leads to a decrease of LCs in neonatal mice and maturation of langerin⁺cells. (A-B) Analysis of neonatal whole skin at defined time points after birth. Cells were pre-gated on viable CD11c⁺ cells. One representative experiment of a 16-day-old neonatal mouse in panel A (n = 5); combined data from at least 6 individually analyzed mice per genotype in panels B and C. (D-F) Increased maturation of p14-deficient, langerin⁺ skin DCs. Whole-skin cells were pre-gated for viable CD11c⁺ cells. Histograms show the expression of CD86 and MHC II on langerin⁺ cells (isotype, gray filled; control, dotted line; CD11c-p14_del, black line). One representative experiment of a 9-day-old neonatal mouse in panel D (n = 5); combined data from 5 individually analyzed mice per genotype in panels E and F. (G) MHC II immunofluorescence staining of epidermal sheets of a 16-day-old CD11c-p14_del mouse, illustrating the disrupted LC network. Skin areas devoid of LCs are indicated with white lines. Scale bar: 200 µm. *P < .05, **P < .01, ***P < .001.