Skip to main content
. 2021 Feb;141(2):404–414.e6. doi: 10.1016/j.jid.2020.06.025

Figure 5.

Figure 5

Tumor progression and epidermal hyperplasia are independent of C3aR1. (a) Tumor susceptibility to DMBA-TPA carcinogenesis in C3ar1–/– (red lines, n = 10) and WT mice (black lines, n = 10). Data are presented as tumor latency, tumor incidence, and tumor area. Statistical analysis of tumor latency was by Mantel‒Cox test and tumor load by linear regression; P-values are indicated. Data representative of two independent experiments are shown. (b) H&E stained ear skin after treatment with 4×TPA in WT (n = 5) and C3ar1−/− (n = 6) mice with quantification of epidermal thickness. Bar = 200 μm. (c) Representative immunofluorescence of C3d (red) and F4/80 (green) in DMBA-TPA‒induced mouse cSCC. Nuclei are counterstained with Hoescht 33342 (gray). Bar = 200 μm. (d) Representative immunofluorescent micrographs of C3d (red) and CD163 (green) staining in human cSCC (n = 5) and normal skin (n = 2). Nuclei are counterstained with DAPI (gray). Original magnification is ×200. cSCC, cutaneous squamous cell carcinoma; DMBA, 7,12-dimethylbenz[a]anthracene; TPA, 12-O-tetradecanoylphorbol-13-acetate; WT, wild type.