目前认为银屑病的发病主要为T细胞介导的以角质形成细胞（KC）为靶点的免疫应答反应。CCL27/CCL28及受体CCR10参与银屑病的发生。课题组前期研究证明IL-22在银屑病KC异常增殖中发挥作用。我们推测IL-22可能通过调控KC中CCL27/CCL28和Th22细胞上受体CCR10的表达参与银屑病的发病。本研究运用分子生物学，免疫学和细胞生物学等，以临床标本、培养的KC和Th22细胞、3D皮肤体外模型和动物模型为研究对象，检测银屑病患者CCL27/CCL28及受体CCR10的表达，检测IL-22、CCL27/CCL28干预前后KC和Th22细胞功能及信号通路的改变，检测IL-22干预前后CCL27/CCL28及受体CCR10表达及相关信号通路的改变，观察3D皮肤体外模型和银屑病动物模型表皮形态及皮肤炎症浸润的改变，意欲阐明CCL27/CCL28及受体CCR10在银屑病发病中的作用。

Psoriasis is a common skin disease with unclear etiology that involves dysregulated interplay between immune cells and keratinocytes. Cutaneous T cell-attracting chemokine (CTACK/CCL27) and mucosae-associated epithelial chemokine (MEC)/CCL28, that promotes migration of lymphocytes into the skin. The role of CCL27,CCL28 and CCR10 in pathogenesis of psoriasis has recently been documented but no data are available at the present time on the related mechanism in keratinocyte hyperproliferation in psoriasis. Interleukine-22 (IL-22) plays an important role in keratinocyte hyperproliferation in psoriasis, as demonstrated by our previous studies. In this study, we will use lesional skin samples and peripheral blood collected from psoriatic patients, cultured keratinocytes, cultured Th22 cells, cultured skin 3D model and a mouse model as our experimental systems. Cultured keratinocytes, skin 3D culture and mice will be treated with IL-22 and IL-22 receptor siRNA or with CCL27,CCL28 and CCR10 proteins. We will use ELISA to detect CCL27,CCL28 and CCR10 in the peripheral blood of psoriatic patients, use real time quantitative RT-PCR to detect CCL27, CCL28 and CCR10 mRNA, use immunohistochemistry and Western-blot to detect CCL27,CCL28 and CCR10 protein. We will also observe epidermal changes in our cultured skin 3D model and mouse model after treatment. We will analyze the relationship between the expression levels of CCL27,CCL28 and CCR10 and severity of psoriasis. The objective of our study is to investigate the role and mechanisms of CCL27,CCL28 and CCR10 functions in keratinocyte hyperproliferation and inflammmatory infiltration in psoriasis. This will help to establish the groundwork for elucidating psoriatic pathogenesis.