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Similar findings were documented in the Cstc−/− mouse ear skin.

Similarly, we analyzed the role of Jak3 in regulating LC migration using a mouse ear skin model.

Micro-projection arrays dry-coated with vaccine material (Gardasil®) delivered to C57BL/6 mouse ear skin released vaccine within 5 minutes.

In the epidermis of Cstc−/− mouse ear skin, we detected significantly more Ki67-positive cells than in that of the Cstc+/+ mice (Figure 8B).

To investigate whether the synergistic actions of rMCP-1 as a recruitment factor for macrophages and PL as a macrophage-activating protein may result in psoriasiform skin inflammation, we simultaneously injected PL and rMCP-1 in mouse ear skin.

In contrast, apoptotic cells from the Cstc+/+ mouse ear skin clustered in the dermis, while ear skin from the Cstc−/− mice had significantly reduced levels of such apoptotic cells (Figure 8A).

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As a source of starting material, we used either embryonic day 14.5 (E14.5) mouse embryonic fibroblasts (MEFs) or mouse adult ear skin fibroblasts (MAFs).

Along with increased γ2 production in Cstc−/− mouse chest and ear skin, we observed significant enhancement of CD31-positive microvessels in the skin of these mice, more than twice as many as those from Cstc+/+ mice (Figure 9B).

However, the human skin is thicker than mouse skin (e.g., mouse ear epidermis is 17.5±2.1 µm [21]; while a candidate vaccination site for humans is the forearm, with a dorsal epidermis is 61.3±11.0 µm [33]).

Further analysis of the ear skin of mice treated with PL and rMCP-1 demonstrated a significant increase of acanthosis when compared with controls (Figure 3G).

According to present findings where significant results were obtained at 1000 mg/kg and 2000 mg/kg doses of extract (Table 4), it can be easily hypothesized that the leaf extract of M. repandus may exhibit anti-inflammatory activity through inhibiting xylene induced inflammatory response and thus ultimately decreases vasodilation and edematous condition of the ear skin of mice.

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