Department of Dermatology, University of Munich, Munich, Germany.
J Eur Acad Dermatol Venereol. 2010 Oct;24 Suppl 6:1-4. doi: 10.1111/j.1468-3083.2010.03829.x.
For many years, psoriasis was firmly believed to be a disease of epidermal keratinocytes, but now is attributed to a combination of genetic and environmental factors that promote a T-cell mediated immune response in the skin. Psoriasis is now understood to be a systemic T-cell mediated autoimmune disease with the innate immune system playing an important role. Progress in understanding the pathogenesis of psoriasis has shown that following a stimulus, dendritic and T cell activation leads to the release of cytokines, chemokines and growth factors that initiate the proliferation and altered differentiation of keratinocytes. These factors subsequently lead to continuous activation of T cells and antigen-presenting cells, particularly dendritic cells, within the psoriatic plaque. This vicious cycle of psoriasis, in which the cytokines interleukin 12 (IL-12) and IL-23 play a pivotal role, is a logical target for biological therapy.
多年来，人们一直坚信银屑病是一种表皮角质形成细胞的疾病，但现在归因于遗传和环境因素的结合，这些因素促进了皮肤中的 T 细胞介导的免疫反应。现在人们认为银屑病是一种系统性 T 细胞介导的自身免疫性疾病，固有免疫系统起着重要作用。对银屑病发病机制的研究进展表明，在受到刺激后，树突状细胞和 T 细胞的激活导致细胞因子、趋化因子和生长因子的释放，从而启动角质形成细胞的增殖和异常分化。这些因子随后导致银屑病斑块内的 T 细胞和抗原呈递细胞（特别是树突状细胞）的持续激活。在这种银屑病的恶性循环中，细胞因子白细胞介素 12（IL-12）和 IL-23 起着关键作用，是生物治疗的合理靶点。
