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Activation and inhibition of mediator release from skin mast cells: a review of in vitro experiments

Mast cells are a physiological cell component of the dermal skin with a high density of about 7000 cells/ mm' and morphological correlation to connective tissue surrounding blood vessels, lymphatic structures, skin appendages and nerves [I], Recently published investigations demonstrated that skin mast cells might develop from pluripotent haematopoeitic stem stells and differentiate by the influence of local growth factors and by functional interaction with fibroblasts [2]. This may at least in part be mediated by stem cell factor (c-kit ligand) which binds to the transmembrane receptor c-kit [2]. Today, it is generally accepted that mast cells (and basophils) are part of complicated cutaneous immune responses [3-5]. These cells express the high affinity IgE receptor (Fe, RI) and are thus involved in IgE-mediated skin diseases such as hymenoptera venom allergies or cutaneous allergic drug reactions. However, their potent (pro)inflammatory mediators which are either released from the characteristic cytoplasmatic granules or newly generated after cell activation (Table I) also appear to be involved in the pathogenesis of a variety of different IgE-independent processes (Table 2). The pattern of mediators and the putative functional interaction with other skin components implicate the clinical use of specific drugs to inhibit the activation of skin mast cells [10]. These cells might therefore be interesting targets for creating new therapeutic strategies. Most important for this aim is to increase our knowledge of the intracellular pathways following stimulus-secretion coupling. The development of enzymatic dispersion techniques to isolate mast cells from human skin allows biochemical and pharmacological characterization of skin mast cells in order to identify the exact mechanisms of secretion. Most authors have used the combination of collagenase and hyaluronidase to remove the cells from different