Kayseri Health Training and Research Center, Dermatology and Venereology Clinic, University of Health Science, Kayseri, Turkey.
Dermatol Ther. 2019 May;32(3):e12916. doi: 10.1111/dth.12916. Epub 2019 Apr 25.
Etiology of psoriasis is unclear but environmental, genetic, and immune factors act significant roles in the pathogenesis of this disease. Helper T cells (TH), plasmoid, and dermal dendritic cells play a prominent role in the development of classical psoriatic lesions. Interleukin stimulation is another important process in the pathogenesis of the disease that directly influences keratinocytes and leading to the formation of psoriatic pattern in the skin. Tumor necrosis factor (TNF) α which releases from keratinocytes activates dendritic cells in the early stages of complex pathogenesis of psoriasis. Activated keratinocytes also produce other proinflammatory cytokines (IL-1b and IL-6), antimicrobial peptides, and various chemokines. TNF activates dendritic cells that produce IL-23, leading to TH17 differentiation. TH17 cells secrete IL-17A, which has been shown to promote psoriatic skin changes. Consequently, after clarification of these main pathological mechanisms, anti-IL therapies have been accepted as a major treatment for patients with moderate-to-severe psoriasis. Here, actual information will be presented about biological agents currently in clinical use or being tested for clinical application for treatment of patients with psoriasis.
银屑病的病因尚不清楚，但环境、遗传和免疫因素在该病的发病机制中起重要作用。辅助性 T 细胞（TH）、浆细胞和真皮树突状细胞在经典银屑病皮损的发展中起突出作用。白细胞介素刺激是疾病发病机制中的另一个重要过程，它直接影响角质形成细胞，导致皮肤出现银屑病样模式。肿瘤坏死因子（TNF）α从角质形成细胞释放出来，在银屑病复杂发病机制的早期阶段激活树突状细胞。活化的角质形成细胞还产生其他促炎细胞因子（IL-1b 和 IL-6）、抗菌肽和各种趋化因子。TNF 激活树突状细胞产生 IL-23，导致 TH17 分化。TH17 细胞分泌 IL-17A，已证明其可促进银屑病皮肤变化。因此，在阐明这些主要病理机制后，抗-IL 治疗已被接受为中重度银屑病患者的主要治疗方法。在这里，将介绍目前正在临床使用或正在进行临床试验以治疗银屑病患者的生物制剂的实际信息。
