Fundación Banco Bilbao Vizcaya Argentaria (F-BBVA)-CNIO Cancer Cell Biology Program, Centro Nacional de Investigaciones Oncológicas, Melchor Fernández Almargo 3, 29029 Madrid, Spain.
Nat Rev Rheumatol. 2010 Dec;6(12):704-14. doi: 10.1038/nrrheum.2010.157. Epub 2010 Sep 28.
Psoriasis is a common inflammatory skin disease of unknown etiology, for which there is no cure. This heterogeneous, cutaneous, inflammatory disorder is clinically characterized by prominent epidermal hyperplasia and a distinct inflammatory infiltrate. Crosstalk between immunocytes and keratinocytes, which results in the production of cytokines, chemokines and growth factors, is thought to mediate the disease. Given that psoriasis is only observed in humans, numerous genetic approaches to model the disease in mice have been undertaken. In this Review, we describe and critically assess the mouse models and transplantation experiments that have contributed to the discovery of novel disease-relevant pathways in psoriasis. Research performed using improved mouse models, combined with studies employing human cells, xenografts and patient material, will be key to our understanding of why such distinctive patterns of inflammation develop in patients with psoriasis. Indeed, a combination of genetic and immunological investigations will be necessary to develop both improved drugs for the treatment of psoriasis and novel curative strategies.
银屑病是一种病因不明的常见炎症性皮肤病，目前尚无治愈方法。这种异质性的皮肤炎症性疾病临床上表现为明显的表皮过度增生和独特的炎症浸润。免疫细胞和角质形成细胞之间的串扰导致细胞因子、趋化因子和生长因子的产生，被认为介导了这种疾病。鉴于银屑病仅在人类中观察到，人们已经采用了多种遗传方法来在小鼠中模拟这种疾病。在这篇综述中，我们描述并批判性地评估了有助于发现银屑病中新的疾病相关途径的小鼠模型和移植实验。使用改良的小鼠模型进行的研究，结合使用人类细胞、异种移植物和患者材料进行的研究，将是我们理解为什么银屑病患者会出现如此独特的炎症模式的关键。事实上，遗传和免疫研究的结合将是开发治疗银屑病的改良药物和新的治愈策略的必要条件。
