Neither injection of rJE/MCP-1 nor rTNF-α alone resulted in psoriasiform skin disease (Supplemental Figure 3 and data not shown). (A and B) A combination of 0.2 μg murine rJE/MCP-1 and 5,000 U rTNF-α, injected in 200 μl PBS intradermally in the upper back skin of nonaffected CD18^hypo PL/J mice (A), led to the appearance of erythematous plaques covered with scales and crusts starting at day 4 after administration (B). (C and D) Skin samples from paraffin sections were stained with H&E before (C) and 10 days after treatment, when epidermal hyperplasia and an abundant inflammatory infiltrate were observed within the dermis (D). (E and F) Cryosections from skin samples before (E) and after treatment stained for the keratinocyte marker K14–Alexa 488 (green) showed an increase in epidermal thickness and enhanced expression of the K14 proliferation-associated marker 10 days after treatment (F). (G and H) At this same time point, a dermal inflammatory infiltrate predominantly consisting of F4/80–Alexa 488⁺– (green) and TNF-α–PE⁺–activated (red) macrophages (overlay, yellow) was identified (H) compared with day 0 (G). (I and J) Interestingly, virtually no CD4-FITC⁺ T cells (green) were present in the dermis before (I) or after treatment with rMCP-1 and rTNF-α (J). Cell nuclei were counterstained with DAPI (blue). Dotted lines indicate the border between epidermis and dermis. Original magnification, ×20.