Psoriasis is a chronic inflammatory autoimmune disease with undefined etiology. Chemokine-like factor 1 (CKLF1), a human cytokine that is a functional ligand for CCR4, displays chemotactic activities in a wide spectrum of leukocytes and plays an important role in psoriasis development. In previous study, our laboratory found that the expression of CKLF1 increased in psoriatic lesions. C19 as a CKLF1's C-terminal peptide has been reported to exert inhibitory effects on a variety of diseases. However, the protective roles of C19 in endothelial cells proliferation and inflammatory cells chemotaxis remain elusive in psoriasis. In this study we examined the protective effect of C19 on both the cellular model and the animal model. The effects of C19 on endothelial cells proliferation and inflammatory cells chemotaxis were investigated in cultured human umbilical vein endothelial cells (HUVECs) and imiquimod-induced psoriasiform inflammation of BALB/c mice based on techniques including immunohistochemical analysis, quantitative real-time PCR (qRT-PCR), western blot, transwell, and EdU assay. This study shows that CKLF1-C19 significantly protects against psoriasis by inhibiting the infiltration of inflammatory cells and proliferation of microvascular cells, possibly via inhibiting MAPK pathways.

中文翻译：

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C19是CKLF1的C末端肽，可减少牛皮癣中皮肤毛细血管的炎症和增殖。

银屑病是一种病因不明的慢性炎性自身免疫性疾病。趋化因子样因子1（CKLF1）是一种人类细胞因子，是CCR4的功能性配体，在广泛的白细胞中显示趋化活性，并在牛皮癣发展中起重要作用。在先前的研究中，我们的实验室发现CKLF1在银屑病皮损中的表达增加。据报道，C19作为CKLF1的C末端肽对多种疾病具有抑制作用。然而，在牛皮癣中，C19在内皮细胞增殖和炎性细胞趋化性中的保护作用仍然难以捉摸。在这项研究中，我们检查了C19对细胞模型和动物模型的保护作用。基于免疫组织化学分析，定量实时PCR（qRT-q）技术，研究了培养的人脐静脉内皮细胞（HUVEC）和咪喹莫特诱导的BALB / c小鼠银屑病炎症中C19对内皮细胞增殖和炎症细胞趋化性的影响。 PCR），蛋白质印迹，transwell和EdU分析。这项研究表明，CKLF1-C19可能通过抑制MAPK途径来抑制炎症细胞的浸润和微血管细胞的增殖，从而有效地预防牛皮癣。