Morioka S, Naito K, Ogawa H
J Invest Dermatol. 1981 May;76(5):337-41. doi: 10.1111/1523-1747.ep12519988.
The pathogenic role of pemphigus autoantibodies and proteinases in epidermal acantholysis has been studied in organ cultures of normal human skin. Dose-dependent acantholysis occurred in skin explants cultured in medium containing 2-30 mg/ml of gamma-globulin from pemphigus serum. Acantholysis was not seen in explants cultured with 2 mg/ml pemphigus gamma-globulin although antibody binding to the epidermis was observed. Some degenerative changes in addition to acantholysis were present when 30 mg/ml pemphigus gamma-globulin was added to the medium. The addition of N,ethylmaleimide(NEM) and ethylene diamine tetraacetate(EDTA) prevented binding of pemphigus antibody to epidermis in culture. Soybean trypsin inhibitor and pepstatin had no effect on binding of pemphigus antibody to the epidermis but they did inhibit acantholysis in vitro. Our results suggest that pemphigus-induced acantholysis may be caused by at least 2 different types of enzyme.
天疱疮自身抗体和蛋白酶在表皮棘层松解中的致病作用已在正常人皮肤器官培养中进行了研究。在含有2-30mg/ml天疱疮血清γ球蛋白的培养基中培养的皮肤外植体中发生了剂量依赖性棘层松解。在用2mg/ml天疱疮γ球蛋白培养的外植体中未观察到棘层松解，尽管观察到抗体与表皮结合。当向培养基中添加30mg/ml天疱疮γ球蛋白时，除了棘层松解外还存在一些退行性变化。添加N-乙基马来酰亚胺（NEM）和乙二胺四乙酸（EDTA）可防止培养中天疱疮抗体与表皮结合。大豆胰蛋白酶抑制剂和胃蛋白酶抑制剂对天疱疮抗体与表皮的结合没有影响，但它们确实在体外抑制了棘层松解。我们的结果表明，天疱疮诱导的棘层松解可能由至少2种不同类型的酶引起。
