The clinical-experimental provocation of blistering and the spontaneous appearance of bullous dermatoses justify the following conclusions: (1) The subcorneal blistering is caused by (a) colloid-osmotic pressure and (b) damaging the membrane of epidermal cells by the toxic influence of enzymes and the chemotactic stimulus on blood cells. (2) The intraepidermal blistering occurs, additionally to (1), by loosening the contact of keratinocytes through irritation of desmosomes and of the plasmalemma, depending on the amount of the doses of the provocating substances, as cantharidin. The morphokinetics of pemphigus vulgaris in comparison with the effect of artificially created intraepidermal blisters (cantharidin) show similarities only in the location but not in the microcellular characteristics. (3) The junction blister, located between basal lamina and basal cells, develops through blocking of enzymes by disturbances of the general metabolism as illustrated by the blistering caused through monoiodoacetate, yellow cross or intracutaneous injection of proteolytIc enzymes. The exchange of fluid of the microcirculation together with viscosity changes within the area of the basal membrane is of importance. (4) The subepidermal blistering, which develops beneath the basal lamina, originates from (a) damage of anchoring fibrils and (b) perivascular edema. This situation leads to blistering in varying layers of the skin combined with autolysis and general liquefaction with regard to separation. (5) The disturbed function of the membrane, especially within the epidermis, leads to a diffusion of the intracellular enzymes (lysosomes), including electrolytes, towards the extracellular space. The active transport against the concentration gradient is missing. (6)The principles of the Koebner phenomena can be demonstrated by chemical vesicants. The limitation in the process of blistering to the subbasal layers only (as in dermatitis herpetiformis Duhring) can be concluded from the increased resistance of the epidermis to the blistering substance as cantharidin). (7) The appearance of spontaneous bullous dermatoses as pemphigus or pemphigoid is closely related to the presence of antibodies and aggressive C’ factors in the blood with corresponding titers. (8) From the viewpoint of therapy, drugs which stabilize the endothelial membranes of the microvessels and diminish the exchange of fluid towards the interstitial area are effective. The immunosuppressive action of such drugs in spontaneous bullous diseases is obviously fundamenta