Autoeczematization is associated with abnormal immune recognition of autologous skin antigens.

Abstract

The pathogenesis of autoeczematization (AE) is not well understood; however, previous studies suggest that AE is an autoimmune condition. Our purpose was to assess whether AE is associated with an abnormal immune recognition of autologous skin antigens. Eight patients with AE, six healthy control subjects, and three patients with localized contact dermatitis (LCD) were studied. Activation markers were detected on peripheral blood T lymphocytes. Autologous mixed epidermal cell-lymphocyte reaction (AMECLR) was performed for each subject and cell proliferation was assessed by tritiated thymidine incorporation. Many activated T cells were detected in patients with AE (5.2% +/- 4.5% vs 0.2% +/- 0.4% in control subjects, p < 0.05). AMECLR showed a significantly higher cell proliferation in AE compared with both healthy subjects and patients with LCD (6372 +/- 3217 cpm vs 2638 +/- 1788 cpm, and 2471 +/- 1389 cpm, respectively; p < 0.05). Peripheral blood mononuclear cells cultured in the presence of an autologous skin homogenate also showed a significantly increased cell proliferation in patients with AE than in control subjects. Our results suggest that an abnormal immune response against autologous skin antigens occurs in AE that could be related to the pathogenesis of this disease.