Ghoreschi Kamran, Weigert Christina, Röcken Martin
Department of Dermatology, Eberhard Karls University Tübingen, 72076 Tübingen, Germany.
Clin Dermatol. 2007 Nov-Dec;25(6):574-80. doi: 10.1016/j.clindermatol.2007.08.012.
Psoriasis is a T cell-dependent autoimmune disease of the skin and joints. Disease manifestation is orchestrated by proinflammatory CD4-positive T helper cells producing either interferon-gamma (Th1) or interleukin (IL)-17 (Th17). These Th1 and Th17 cells interact with dermal dendritic cells, macrophages, mast cells, and neutrophils. Together, they cause an inflammation that mainly involves interferon-gamma, tumor necrosis factor, IL-8, IL-12, IL-17, IL-19, and IL-23. New therapeutics either are directed against T cells, tumor necrosis factor, and IL-12/IL-23 or deviate immune responses into a protective IL-4-dominated Th2 phenotype.
银屑病是一种皮肤和关节的T细胞依赖性自身免疫性疾病。疾病表现由产生干扰素-γ（Th1）或白细胞介素（IL）-17（Th17）的促炎性CD4阳性辅助性T细胞精心编排。这些Th1和Th17细胞与真皮树突状细胞、巨噬细胞、肥大细胞和中性粒细胞相互作用。它们共同引发一种炎症，主要涉及干扰素-γ、肿瘤坏死因子、IL-8、IL-12、IL-17、IL-19和IL-23。新的治疗方法要么针对T细胞、肿瘤坏死因子和IL-12/IL-23，要么将免疫反应转变为以保护性IL-4为主导的Th2表型。
