Investigation on the mechanisms of skin residual deneritic cells in the development psoriasis vulgaris.

银屑病是一种常见的慢性炎症性皮肤病，涉及免疫细胞和角质形成细胞之间的相互作用失调。朗格汉斯细胞（LC）是树突状细胞的一个子集，位于表皮中并调节免疫反应。在这项研究中，我们专注于Th 17相关因子，并评估了LC和γ-δ T细胞在银屑病发展中的作用，使用由局部应用咪喹莫特（IMQ）引发的小鼠银屑病模型。在Langerin DT受体敲入小鼠中，通过白喉毒素（DT）消除朗格汉斯细胞抑制了IMQ处理区域的角化过度、角化不全和耳肿胀。此外，LC耗竭小鼠在IMQ治疗的皮肤病变中显示出Th 17相关细胞因子水平降低。这些结果表明，LCs是由IMQ诱导的小鼠银屑病样病变的发展所必需的。

Psoriasis is a common chronic inflammatory skin disease that involves dysregulated interplay between immune cells and keratinocytes. Langerhans cells (LCs) are a subset of dendritic cells that reside in the epidermis and regulate immune responses. In this study, we focused on Th17-related factors and assessed the role of LCs and gamma-delta T cells in the development of psoriasis using a mouse psoriasis model triggered by topical application of imiquimod (IMQ). Langerhans cell depletion by means of diphtheria toxin (DT) in Langerin DT receptor-knocked-in mice suppressed hyperkeratosis, parakeratosis and ear swelling in the IMQ-treated regions. In addition, LC-depleted mice showed decreased levels of Th17-related cytokines in IMQ-treated skin lesions. These results suggest that LCs are required for the development of psoriasis-like lesions induced by IMQ in mice.