Etiology and Pathogenesis of Psoriasis
Etiology and Pathogenesis of Psoriasis
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DOI：
10.1016/j.rdc.2015.07.013
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发表时间：
2015-11-01
影响因子：
2.3
通讯作者：
Boehncke, Wolf-Henning
中科院分区：
文献类型：
--
作者：
Boehncke, Wolf-Henning
牛皮癣是一种常见的慢性炎症性皮肤病，通常以边界清楚的鳞片斑块的形式出现。这些损害突出了其发病的基本过程，即炎症和表皮过度增殖。这两种现象都被认为是先天免疫系统和获得性免疫系统之间密切相互作用的结果。这一概念得到了遗传学研究结果的支持，指出核因子-kappa B、干扰素-γ和白介素23的信号通路以及抗原提呈是银屑病炎症的中心轴。针对肿瘤坏死因子-α、IL-23或IL-17的生物制剂的有效性提供了支持这一模式的进一步证据。
Psoriasis is a common, chronic inflammatory skin disease most often appearing in the form of well-demarcated, scaly plaques. These lesions highlight the fundamental processes underlying its pathogenesis, namely, inflammation and epidermal hyperproliferation. Both phenomena are considered consequences of an intimate interplay between the innate and the adaptive immune system. This concept is supported by results of genetic studies, pointing toward the signaling pathways of nuclear factor-kappa B, interferon-gamma, and interleukin (IL)-23 as well as antigen presentation as central axes of the psoriatic inflammation. Efficacy of biologics targeting tumor necrosis factor-alpha, IL-23, or IL-17 provides further evidence in favor of this model.