McKenzie R C, Sabin E
Epidermal Inflammation and Protection Group, Department of Dermatology, University of Edinburgh, Edinburgh, Scotland, UK.
Exp Dermatol. 2003 Aug;12(4):337-45. doi: 10.1034/j.1600-0625.2003.00100.x.
Psoriasis is a chronic inflammatory skin disease characterized by the accumulation of red, scaly plaques on the skin. The plaques result from hyperproliferation and incomplete differentiation of keratinocytes (KC) in a process that seems to be driven, in part by skin-infiltrating leucocytes. We believe that the KC have inherent defects in intracellular signalling which could be usefully targeted to allow the development of more effective therapies. We suggest that there are defects in the regulation of the transcription factors: signal transducer and activator of transcription (STAT-1alpha), interferon regulated factor-1 (IRF-1) and NFkappaB which lead to loss of growth and differentiation control when the cells are subjected to physico-chemical and immunological stress. We also highlight recent studies that suggest that peroxisome proliferator-activated receptors, the notch receptor and defects in calcium and other ion transporting proteins may contribute to impairment in the ability of psoriatic KC to differentiate. The role of these systems in the development of the psoriatic phenotype and tests of these hypotheses are proposed.
银屑病是一种慢性炎症性皮肤病，其特征是皮肤上出现红色鳞屑斑块。这些斑块是由角质形成细胞（KC）过度增殖和不完全分化所致，这一过程似乎部分由浸润皮肤的白细胞驱动。我们认为，KC在细胞内信号传导方面存在内在缺陷，这些缺陷可作为有效靶点，以开发更有效的治疗方法。我们认为，转录因子信号转导和转录激活因子（STAT-1α）、干扰素调节因子-1（IRF-1）和核因子κB的调节存在缺陷，当细胞受到物理化学和免疫应激时，会导致生长和分化控制丧失。我们还强调了最近的研究，这些研究表明过氧化物酶体增殖物激活受体、Notch受体以及钙和其他离子转运蛋白的缺陷可能导致银屑病KC分化能力受损。本文提出了这些系统在银屑病表型形成中的作用以及对这些假设的检验。
