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In the other groups, the drug was withdrawn on day 50 and observation was continued until day 65. The results showed that all the mice that received monobenzone developed depigmentation in the exposed area (Fig.?1a). The mice received Vaseline showed no depigmentation (Fig.?1d). The ratio of the mice that developed Fleroxacin distant depigmentation and the severity of depigmentation increased along with the increase in monobenzone concentration (Fig.?1e,f). Depigmentation patches occurred in approximately 20%, 50% and 70% of the mice in groups II, III and IV, respectively (Fig.?1e), when the experiment was completed. The mice in groups II, III and IV had CHIR-99021 mw pigmented keratinocytes, appeared as bright refractive granules under RCM (Fig.?2a). In contrast, the dermal papillary in the skin with depigmentation showed significant decrease in the number of bright granules, suggesting the loss of melanocytes and pigmented keratinocytes (Fig.?2b). Histochemical analysis demonstrated that leukomonocyte infiltration was elevated in the perilesional skin of the distant depigmentation (Fig. S1). Immunofluorescence staining with anti-CD8 antibody revealed that the infiltrated lymphocytes included a substantial amount of CD8+ T cells (Fig.?2c). Only few CD8+ T cells were observed in the healthy skin (Fig.?2d). We treated Rag1 knockout (KO) mice, which have a deficiency in generating mature T cells, with 40% monobenzone cream. In contrast to healthy C57BL/6 click here mice, which developed distant depigmentation beyond the monobenzone-exposed site (Fig.?2f), the Rag1 KO mice developed depigmentation restricted only in the drug exposure area (Fig.?2e). Until now, understanding to the cellular and molecular mechanisms causing melanocyte loss in vitiligo is still unclear, partly due to the limitations of current in vitro research methodologies on vitiligo [8] and the paucity of suitable animal models. Existing mouse models of vitiligo are generally established through specifically expressing exogenic protein in skin melanocytes, leading to the destruction of the melanocytes by CD8+ CTL targeting the exogenic antigen [9-12]. As a consequence, these vitiligo models do not authentically represent the activation mechanism of autoimmune CD8+ T cells in human vitiligo. In this study, we developed a new vitiligo model by topically applying monobenzone.
