Heng M C, Allen S G
Division of Dermatology, VA Medical Center, Sepulveda, California 91343.
Australas J Dermatol. 1991;32(2):93-100. doi: 10.1111/j.1440-0960.1991.tb00073.x.
The pathophysiology and immune mechanisms involved in the clinical syndrome of autoeczematization remain a mystery. In this study of nickel dermatitis without autoeczematization and poison oak dermatitis with autoeczematization, it was noted that the process of autoeczematization was associated with the presence of CD8+ lymphocytes within the epidermis and the expression of HLA-DR antigens on epidermal keratinocytes. It is surmised that since CD8+ clones are induced by poison oak antigen but not by nickel, the inability of nickel to induce CD8+ lymphocytes may explain why uncomplicated nickel dermatitis does not autoeczematize. Since the selective adherence of CD8+ lymphocytes to keratinocytes, probably via the expression of adhesion molecules such as ICAM-1, the generation of antigens on endothelial cells of high endothelial venules involved in lymphocyte trafficking, and the expression of HLA-DR antigens on epidermal keratinocytes are all due to the activity of interferon-8, it is deduced that this lymphokine may play a key role in id eruptions induced by contact allergens.
自体湿疹化临床综合征所涉及的病理生理学和免疫机制仍是个谜。在这项针对无自体湿疹化的镍皮炎和有自体湿疹化的毒橡树皮炎的研究中，注意到自体湿疹化过程与表皮内CD8 +淋巴细胞的存在以及表皮角质形成细胞上HLA - DR抗原的表达有关。据推测，由于CD8 +克隆是由毒橡树抗原而非镍诱导产生的，镍无法诱导CD8 +淋巴细胞这一点或许可以解释为何单纯性镍皮炎不会发生自体湿疹化。由于CD8 +淋巴细胞可能通过ICAM - 1等黏附分子的表达而选择性地黏附于角质形成细胞，参与淋巴细胞运输的高内皮微静脉内皮细胞上抗原的产生，以及表皮角质形成细胞上HLA - DR抗原的表达均归因于干扰素 - 8的活性，因此推断这种淋巴因子可能在接触性变应原诱发的皮疹中起关键作用。
