Autoeczematization is associated with abnormal immune recognition of autologous skin antigens Article uri icon

abstract

  • Background: The pathogenesis of autoeczematization (AE) is not well understood; however, previous studies suggest that AE is an autoimmune condition. Objective: Our purpose was to assess whether AE is associated with an abnormal immune recognition of autologous skin antigens. Methods: 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. Results: Many activated T cells were detected in patients with AE (5.2%25 ± 4.5%25 vs 0.2%25 ± 0.4%25 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. Conclusion: 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. © 1993, American Academy of Dermatology, Inc.. All rights reserved.

publication date

  • 1993-01-01