Department of Dermatology and Department of Immunology, Erasmus MC, University Medical Center, Rotterdam, The Netherlands.
Expert Rev Mol Med. 2009 Dec 14;11:e38. doi: 10.1017/S146239940900129X.
Psoriasis is a chronic inflammatory skin disease characterised by elevated red scaly plaques on specific body sites. Histologically, the plaques are defined by epidermal hyperplasia, epidermal and dermal infiltration by leukocytes, and changes in the dermal microvasculature. Differentiation and activation are disturbed in lesional psoriatic keratinocytes, and the pool of proliferating keratinocytes is increased, which is accompanied by enhanced production of proinflammatory cytokines, adhesion molecules and antimicrobial peptides. These changes in psoriatic keratinocytes are caused by altered expression of genes associated with epidermal differentiation, and by activation of signalling pathways involving signal transducer and activator of transcription 3 (STAT3), type I interferon (IFN) and mitogen-activated protein kinase (MAPK). The number of T cells, and myeloid and plasmacytoid dendritic cells (DCs) is markedly increased in psoriatic lesions. Myeloid DCs produce interleukin (IL)-23, tumour necrosis factor (TNF)-alpha and inducible nitric oxide synthase (iNOS), which are crucial cytokines in the pathogenesis of psoriasis. IL-23 stimulates the secretion of IL-22 by T helper 17 cells, and IL-22 induces epidermal hyperplasia. The crosstalk between keratinocytes and leukocytes via their proinflammatory cytokines creates the vicious circle of chronic skin inflammation seen in psoriasis. This suggests that optimal treatment of psoriasis needs to target pathogenic pathways in both leukocytes and keratinocytes.
银屑病是一种慢性炎症性皮肤病，其特征是在特定身体部位出现红色鳞屑斑块。组织学上，斑块由表皮过度增生、表皮和真皮白细胞浸润以及真皮微血管改变定义。病变银屑病角质形成细胞的分化和激活受到干扰，增殖角质形成细胞池增加，同时伴有促炎细胞因子、黏附分子和抗菌肽的产生增加。这些银屑病角质形成细胞的变化是由与表皮分化相关的基因表达改变以及涉及信号转导和转录激活因子 3（STAT3）、I 型干扰素（IFN）和丝裂原活化蛋白激酶（MAPK）的信号通路激活引起的。在银屑病病变中，T 细胞以及髓样和浆细胞样树突状细胞（DC）的数量明显增加。髓样 DC 产生白细胞介素（IL）-23、肿瘤坏死因子（TNF）-α和诱导型一氧化氮合酶（iNOS），它们是银屑病发病机制中的关键细胞因子。IL-23 刺激辅助性 T 细胞 17 细胞分泌 IL-22，IL-22 诱导表皮过度增生。角质形成细胞和白细胞通过其促炎细胞因子相互作用，形成银屑病慢性皮肤炎症的恶性循环。这表明，银屑病的最佳治疗需要针对白细胞和角质形成细胞中的致病途径。
