Sabat Robert, Philipp Sandra, Höflich Conny, Kreutzer Stefanie, Wallace Elizabeth, Asadullah Khusru, Volk Hans-Dieter, Sterry Wolfram, Wolk Kerstin
Interdisciplinary Group of Molecular Immunopathology, Dermatology/Medical Immunology, University Hospital Charité, Berlin, Germany.
Exp Dermatol. 2007 Oct;16(10):779-98. doi: 10.1111/j.1600-0625.2007.00629.x.
Psoriasis is a chronic skin disease that affects about 1.5% of the Caucasian population and is characterized by typical macroscopic and microscopic skin alterations. Psoriatic lesions are sharply demarcated, red and slightly raised lesions with silver-whitish scales. The microscopic alterations of psoriatic plaques include an infiltration of immune cells in the dermis and epidermis, a dilatation and an increase in the number of blood vessels in the upper dermis, and a massively thickened epidermis with atypical keratinocyte differentiation. It is considered a fact that the immune system plays an important role in the pathogenesis of psoriasis. Since the early 1990s, it has been assumed that T1 cells play the dominant role in the initiation and maintenance of psoriasis. However, the profound success of anti-tumor necrosis factor-alpha therapy, when compared with T-cell depletion therapies, should provoke us to critically re-evaluate the current hypothesis for psoriasis pathogenesis. Recently made discoveries regarding other T-cell populations such as Th17 and regulatory T cells, dendritic cells, macrophages, the keratinocyte signal transduction and novel cytokines including interleukin (IL)-22, IL-23 and IL-20, let us postulate that the pathogenesis of psoriasis consists of distinct subsequent stages, in each of them different cell types playing a dominant role. Our model helps to explain the varied effectiveness of the currently tested immune modulating therapies and may enable the prediction of the success of future therapies.
银屑病是一种慢性皮肤病，影响约1.5%的白种人，其特征为典型的宏观和微观皮肤改变。银屑病皮损为边界清晰、红色且略隆起的皮损，伴有银白鳞屑。银屑病斑块的微观改变包括真皮和表皮中免疫细胞浸润、真皮上层血管扩张和数量增加，以及表皮大量增厚伴非典型角质形成细胞分化。免疫系统在银屑病发病机制中起重要作用，这一点已被公认。自20世纪90年代初以来，人们一直认为T1细胞在银屑病的起始和维持中起主导作用。然而，与T细胞清除疗法相比，抗肿瘤坏死因子-α疗法取得的显著成功应促使我们批判性地重新评估当前关于银屑病发病机制的假说。最近关于其他T细胞群体（如Th17和调节性T细胞）、树突状细胞、巨噬细胞、角质形成细胞信号转导以及包括白细胞介素（IL）-22、IL-23和IL-20在内的新型细胞因子的发现，使我们推测银屑病的发病机制由不同的后续阶段组成，在每个阶段中不同的细胞类型起主导作用。我们的模型有助于解释目前所测试的免疫调节疗法的不同疗效，并可能有助于预测未来疗法的成功。
