Psoriasis is a chronic inflammatory skin disease which mainly involves immune system. This research was to investigate the role of MST1 in the psoriasis, and the detailed mechanism whether related with Th17 and NF-κB. The skin samples and peripheral blood were obtained from psoriasis patients. Skin samples and T cells isolated from peripheral blood of patients were cultured in vitro. The results showed that the level of MST1 in the lesional skin of all three patients was higher than that of un-lesional skin, as well as the amount of CD4, CD8 and IL17 positive T cells. The amount of circulating Th17 was higher than that of control. The level of MST1, IL-17, IL-22 and TNFα was enhanced in activated T cells (p < 0.01), which indicated that MST1 increased markedly in activated T cells. The proliferation and migration of T cells were decreasing in MST1 knockdown cells, while increasing in overexpressed cells, as well as the production of IL-17, IL-22 and TNFα. MST1 enhanced the activation of TLR4-NF-κB signaling pathway, and TLR4 knockdown could reverse the effect of MST1 on NF-κB activation. This research indicated that MST1 could regulate the activation of Th17 in psoriasis partly through TLR4-NF-κB pathway. MST1 may be a target for treatment of psoriasis.

牛皮癣是一种慢性炎症性皮肤病，主要涉及免疫系统。本研究旨在探讨MST1在牛皮癣中的作用，以及其与Th17和NF-κB是否相关的详细机制。皮肤样本和外周血是从牛皮癣患者获得的。从患者外周血中分离出的皮肤样本和T细胞在体外培养。结果表明，三例患者的病变皮肤中的MST1水平均高于非病变皮肤，以及CD4，CD8和IL17阳性T细胞的水平。Th17的循环量高于对照。活化的T细胞中MST1，IL-17，IL-22和TNFα的水平升高（p <0.01），这表明MST1在活化的T细胞中显着增加。T细胞的增殖和迁移在MST1敲低的细胞中减少，而在过表达的细胞中增加，以及IL-17，IL-22和TNFα的产生。MST1增强了TLR4-NF-κB信号通路的激活，而TLR4敲低可以逆转MST1对NF-κB激活的作用。这项研究表明，MST1可以部分通过TLR4-NF-κB途径调节牛皮癣中Th17的活化。MST1可能是治疗牛皮癣的靶标。