Bruckner-Tuderman L
Department of Dermatology, University of Münster, Germany.
Dermatology. 1994;189 Suppl 2:16-20. doi: 10.1159/000246983.
Recent advances in molecular and cell biology of the cutaneous basement membrane zone have drastically increased our knowledge of the pathomechanisms underlying skin blistering disorders. Defects in genes coding for the structural proteins of the basement membrane zone have been defined in epidermolysis bullosa (EB), and abnormal expression of the structural proteins in some of its subtypes. The underlying cause for several subtypes of dystrophic EB are mutations in the gene for collagen VII, COL7A1. In vitro studies utilizing cells derived from the skin of such patients have helped understanding the pathogenetic pathways that lead from the mutation to the symptom, skin blistering. The data accumulated from analyses of the genetic disorders will also yield indirect information on the normal physiology of the skin and be highly relevant for the clarification of the etiopathogenesis of acquired blistering diseases.
皮肤基底膜带分子与细胞生物学的最新进展极大地增加了我们对皮肤水疱性疾病潜在发病机制的认识。在大疱性表皮松解症(EB)中已明确了编码基底膜带结构蛋白的基因突变,并且在其某些亚型中存在结构蛋白的异常表达。营养不良性EB的几种亚型的根本原因是Ⅶ型胶原基因COL7A1的突变。利用此类患者皮肤来源的细胞进行的体外研究有助于理解从突变到症状(皮肤水疱形成)的致病途径。从这些遗传性疾病分析中积累的数据也将产生关于皮肤正常生理学的间接信息,并且对于阐明获得性水疱性疾病的病因发病机制高度相关。