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Abstract：
Psoriasis is a complex chronic inflammatory skin disease caused by the dynamic interplay between multiple genetic risk foci, environmental risk factors, and excessive immunological abnormalities. Psoriasis affects approximately 2% of the population worldwide, and dramatic advances have been achieved in the understanding and treatment options for psoriasis. Recent progress in biological therapies has revealed the fundamental roles of tumor necrosis factor-α, interleukin (IL)-23p19, and the IL-17A axis together with skin-resident immune cells and major signal transduction pathways in the pathogenesis of psoriasis. In addition to IL-17-producing T helper17 cells, innate lymphoid cell (ILC)3 induces psoriasis rashes directly without T-cell/antigen interaction in response to the released antimicrobial peptides from activated keratinocytes and inflammatory cytokines. ILC3 typically expresses retinoic acid receptor-related orphan receptor gamma t in the nucleus, matures in the presence of IL-7 and IL-23, and produces IL-17 and IL-22. The number of ILC3s is increased in the blood, psoriasis rash, and even in nonrash areas of psoriatic skin. Psoriasis is significantly associated with cardiovascular disease, metabolic syndrome, and inflammatory disorders, particularly the severe type. The similarity of enterobacteria in the psoriasis gut to that in diabetic patients may be related to its pathogenesis. In the current review, we focus on the pathophysiology of psoriasis in the accelerated immunological inflammatory loop, danger signal from keratinocytes, and cytokines, particularly IL-17 and IL-23p19. In addition, pathophysiological speculation with regard to morphology has been supplemented. Finally, the differences and similarities between psoriasis and atopic dermatitis are discussed.
摘要：
银屑病是一种复杂的慢性炎症性皮肤病，由多种遗传风险灶之间的动态相互作用引起。环境风险因素，和过度的免疫异常。牛皮癣影响全球约2％的人口，在银屑病的理解和治疗选择方面取得了巨大的进步。生物治疗的最新进展揭示了肿瘤坏死因子-α的基本作用。白细胞介素（IL）-23p19，IL-17A轴与皮肤固有免疫细胞和主要信号转导通路一起在银屑病的发病机制中。除了产生IL-17的Thelper17细胞，先天淋巴样细胞(ILC)3响应活化角质形成细胞和炎性细胞因子释放的抗菌肽,直接诱导银屑病皮疹而无T细胞/抗原相互作用.ILC3通常在细胞核中表达视黄酸受体相关的孤儿受体γt，在IL-7和IL-23存在下成熟,并产生IL-17和IL-22。ILC3的数量在血液中增加，牛皮癣皮疹,甚至在牛皮癣皮肤的非皮疹区域。银屑病与心血管疾病显著相关,代谢综合征,和炎症性疾病，尤其是严重的类型。银屑病肠道中肠杆菌与糖尿病患者肠道中肠杆菌的相似性可能与其发病机制有关。在当前的审查中，我们专注于加速免疫炎症循环中银屑病的病理生理学，来自角质形成细胞的危险信号，和细胞因子，特别是IL-17和IL-23p19。此外,关于形态学的病理生理学推测得到了补充。最后,讨论了银屑病与特应性皮炎的异同。
