Introduction

All organisms are confronted on a daily basis with a wide range of insults like changes in temperature and humidity, UV-light, wounding and exposure to a large number of potentially pathogenic microorganisms. To survive and maintain homeostasis in this hostile environment, higher animals have developed a complex and specialized structure, the skin, which possesses a remarkable capacity to deal with these challenges. The skin primarily provides a barrier that prevents water loss and the entry of adverse environmental agents. This organ also displays thermoregulatory, mechanosensory, immunological and metabolic properties.

The skin is composed of two main compartments, the epidermis and the dermis, which communicate extensively to establish, maintain and restore homeostasis. Keratinocytes provide the basic structure of the epidermis whereas fibroblasts, together with the collagens they produce, form the basic scaffold of the dermis. Both compartments also contain other cell types, such as Langerhans cells,melanocytes and Merkel cells in the epithelial layer and immune cells (dendritic cells, macrophages, mast cells), endothelial cells, adipocytes and muscle cells in the mesenchymal layer. The epidermis and the dermis cooperate in the formation of a highly specialized extracellular matrix structure, the basement membrane zone, which physically spearates these two compartments. In recent years it has become increasingly clear that the different skin cell types have a profound functional influence on each other and that an extensive cellular cross-talk regulates cell proliferation and differentiation and coordinates the cellular responses to environmental challenges.

The complexity of the multifunctional skin barrier system is mirrored by a broad spectrum of distinct skin disease entities, which are caused by failure or dysfunction of different structures and cells of the skin. These include several inborn and acquired diseases in which the coherence of keratinocytes is reduced or their mechanical stability is altered. Others are characterized by defective adhesion of keratinocytes to the dermis due to interference with cellular adhesion receptors or alterations in basement membrane structures. The underlying causes for such hyperkeratotic and/or blistering diseases are either molecular defects in the genes encoding distinct proteins or result from auto-antibodies interfering with cell-cell or cell-matrix interactions. Mutations in certain cytoskeletal proteins have also been shown to result in ichthyosis vulgaris and to be involved in atopic dermatitis and asthma (Bieber et al., 2008).

 

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