Gaspari Anthony A
Department of Dermatology, University of Maryland School of Medicine, Baltimore, Maryland 21201, USA.
J Am Acad Dermatol. 2006 Mar;54(3 Suppl 2):S67-80. doi: 10.1016/j.jaad.2005.10.057.
Psoriasis is considered to be a genetically programmed disease of dysregulated inflammation, which is driven and maintained by multiple components of the immune system. The pathologic collaboration between innate immunity (mediated by antigen-presenting cells and natural killer T lymphocytes) and acquired immunity (mediated by T lymphocytes) results in the production of cytokines, chemokines, and growth factors that contribute to the inflammatory infiltrate seen in psoriatic plaques. This overview of the pathophysiology of psoriasis describes these events, and recent developments that have contributed to our understanding of the role of immune function in psoriasis. These developments include the creation of useful animal models and identification of new receptors and lymphocyte subtypes that may participate in the development of this chronic disease.
银屑病被认为是一种炎症调节失调的基因程序性疾病，由免疫系统的多个成分驱动和维持。先天免疫（由抗原呈递细胞和自然杀伤T淋巴细胞介导）和后天免疫（由T淋巴细胞介导）之间的病理协作导致细胞因子、趋化因子和生长因子的产生，这些因子促成了银屑病斑块中所见的炎症浸润。本文对银屑病病理生理学的概述描述了这些事件，以及有助于我们理解免疫功能在银屑病中作用的最新进展。这些进展包括创建有用的动物模型，以及识别可能参与这种慢性疾病发展的新受体和淋巴细胞亚型。
