Fitch Erin, Harper Erin, Skorcheva Iliyana, Kurtz Stephen E, Blauvelt Andrew
Dermatology Service, Veterans Affairs Medical Center, 3710 Southwest US Veterans Hospital Road, Mail Code R&D 55, Portland, OR 97239, USA.
Curr Rheumatol Rep. 2007 Dec;9(6):461-7. doi: 10.1007/s11926-007-0075-1.
T helper (Th) 17 cells, a novel T-cell subset, have been implicated in the pathogenesis of psoriasis and other autoimmune inflammatory diseases. Interleukin (IL)-23 stimulates survival and proliferation of Th17 cells, and thus serves as a key master cytokine regulator for these diseases. In psoriasis, IL-23 is overproduced by dendritic cells and keratinocytes, and this cytokine stimulates Th17 cells within dermis to make IL-17A and IL-22. IL-22, in particular, drives keratinocyte hyperproliferation in psoriasis. Future targeting of these key cytokines is likely to lead to dramatic clinical improvement in patients with psoriasis. This review focuses on the numerous recent studies on the roles of IL-23 and Th17 cells in the pathogenesis of psoriasis.
辅助性T(Th)17细胞是一种新型T细胞亚群,与银屑病及其他自身免疫性炎症性疾病的发病机制有关。白细胞介素(IL)-23可刺激Th17细胞存活和增殖,因此是这些疾病的关键主要细胞因子调节因子。在银屑病中,树突状细胞和角质形成细胞过度产生IL-23,这种细胞因子刺激真皮内的Th17细胞产生IL-17A和IL-22。特别是IL-22可促使银屑病中的角质形成细胞过度增殖。未来针对这些关键细胞因子进行治疗可能会使银屑病患者的临床症状得到显著改善。本综述重点关注了近期关于IL-23和Th17细胞在银屑病发病机制中作用的众多研究