ERYTHEMA MULTIFORME: A CLINICAL PATHOGENETIC STUDY

多形性红斑是一种急性综合征，常发生在感染后。 我们 初步的临床发病机制研究表明， 单纯疱疹病毒感染的多形性隐球菌。 我们 关于单纯疱疹相关红斑发病机制的假说 多形性是它涉及免疫复合物的形成。 我们认为 疱疹相关性多形性红斑可能是原位免疫复合物模型 阵 如果疱疹糖蛋白抗原被释放到血液循环中， 这些患者，他们倾向于与 表皮细胞表面。 由于疱疹病毒是表皮营养性的， 蛋白质参与病毒与表皮细胞膜的结合， 细胞 随后抗体与膜结合抗原的结合可能 导致表皮细胞的破坏，如在多形性红斑中所见。 我们计划利用酶免疫测定和免疫荧光技术， 评估循环免疫复合物和皮肤中的HSV抗原和抗体 从多形性红斑患者获得的活组织检查。

Erythema multiforme is an acute syndrome often following an infection. Our preliminary clinical pathogenetic study has demonstrated a high association of erythemia multiforme with preceding herpes simplex virus infection. Our hypothesis regarding the pathogenesis of herpes simplex-associated erythema multiforme is that it involves immune complex formation. We believe that herpes-associated erythema multiforme may pose a model of in situ immune complex formation. If herpes glycoprotein antigens are released into the circulation of these patients, it would seem reasonable that they would tend to bind to the surface of epidermal cells. Since herpes viruses are epidermotrophic these proteins are involved in the binding of the virus to the membrane of epidermal cells. Subsequent combinations of antibody with membrane-bound antigen might lead to destruction of cells in the epidermis as seen in erythema multiforme. We plan to utilize enzyme immunoassays and immunofluorescent techniques to evaluate HSV antigens and antibodies in circulating immune complexes and skin biopsies obtained from erythema multiforme patients.