Figure 6
Figure 6. Inflammatory cell infiltration during acute skin inflammation. (A-D) Immunofluorescence analyses for the monocyte/granulocyte marker CD11b and subsequent computer-based quantification showed a significantly increased number of dermal CD11b+ cells per millimeter basement membrane (BM) 2 days after oxazolone challenge (2 days oxa, A,C; ear skin) or UVB irradiation (2 days UVB, B,D; back skin) in K14-VEGF-C, K14-VEGF-D Tg, and wild-type mice, compared with untreated mice of the same genotype. K14-VEGF-C Tg mice had even more infiltrated dermal CD11b+ cells in their ear skin 2 days after oxazolone challenge compared with oxazolone challenged wild-type mice (A,C). The hair follicle sebaceous glands are stained red (C-D) because of endogenous biotin. (A-D) Data are mean ± SD. ***P ≤ .001. ns indicates not significant versus oxazolone challenged or UVB-irradiated wild-type mice. Bars represent 100 μm (C), 50 μm (D).

Inflammatory cell infiltration during acute skin inflammation. (A-D) Immunofluorescence analyses for the monocyte/granulocyte marker CD11b and subsequent computer-based quantification showed a significantly increased number of dermal CD11b+ cells per millimeter basement membrane (BM) 2 days after oxazolone challenge (2 days oxa, A,C; ear skin) or UVB irradiation (2 days UVB, B,D; back skin) in K14-VEGF-C, K14-VEGF-D Tg, and wild-type mice, compared with untreated mice of the same genotype. K14-VEGF-C Tg mice had even more infiltrated dermal CD11b+ cells in their ear skin 2 days after oxazolone challenge compared with oxazolone challenged wild-type mice (A,C). The hair follicle sebaceous glands are stained red (C-D) because of endogenous biotin. (A-D) Data are mean ± SD. ***P ≤ .001. ns indicates not significant versus oxazolone challenged or UVB-irradiated wild-type mice. Bars represent 100 μm (C), 50 μm (D).

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