ABSTRACT
Another major mechanism for causing such weakening is genetic mutation. When one or more of these connecting components are formed in a dysfunctional manner, leading to structural weakening, blistering results [5]. Conversely, restoring the expression of these dysfunctional structures by gene correction or by protein delivery results in normal skin structure and function [3; 6]. Several groups of heritable blistering skin diseases in this category include epidermolysis bullosa simplex, junctional epidermolysis bullosa, and epidermolysis bullosa dystrophica, which are caused by mutations in geneencoding plectin/keratins 5 & 14, laminin-5/BP180/ 64 integrin, and type-VII collagen, respectively. The third major mechanism for inducing such weakening is toxin from infectious organisms. When these connecting components are directly attacked by these toxins, resulting in structural weakening, blisters surface. One of the best-known examples, bullous impetigo, and its generalized form, staphylococcal scalded-skin syndrome, have recently been determined to be the direct result of enzymatic cleavage of desmoglein 1 by the actions of staphylococcal exfoliative toxins A & B [4].
