The aim of this review is to summarize recent knowledge about the structure and components of dermoepidermal junction and about the role of these structures in pathogenesis of genetic and acquired blistering diseases localized to the junction zone. Hemidesmosome is the crucial structure that contributes to the attachment of keratinocytes to the dermis. The hemidesmosome molecules mediate signals co-ordinating the attachment of cells, their survival, growth and migration. Hemi- desmosome is composed of four known molecules - bullous pemphigoid antigens BP1 and BP2, plectin and a6b4 integrin. Antibodies against hemidesmosome and other components of dermoepidermal junction cause autoimmune blistering diseases. Genetic mutations of these molecules result in genetic blistering diseases.

        Key words: hemidesmosome - basement membrane - bullous pemphigoid - epidermolysis