Lack of expression of intercellular adhesion molecule ICAM-1 in lepromatous leprosy patients.

It is conceivable that an abnormal expression of cell-adhesion molecules can contribute to the poor inflammatory response seen in some inflammatory skin diseases. Adhesins are cell-surface molecules that are expressed by many cell types. The main function of adhesins appears to be the promotion of cellular interactions, such as those occurring between immune cells. The epidermis of patients with inflammatory skin diseases exhibits an increased expression of ICAM-1, and it has been postulated that such increased expression can be important in the genesis of cutaneous inflammation. The expression of cell-adhesion molecules (LFA-1, LFA-2, LFA-3 and ICAM-1) in skin lesions of leprosy patients was studied, as well as the in vitro expression of these molecules induced with gamma interferon (IFN-gamma). A lack of expression of ICAM-1 in the epidermis of lepromatous patients was noted; in addition, no expression of ICAM-1 was seen in the nearly normal skin from these patients incubated with IFN-gamma. A similar expression of the four molecules studies was noted in the dermis of both the lepromatous and tuberculoid types of leprosy. The epidermis of the lepromatous leprosy patients appears to have a defective expression of ICAM-1.

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

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% +/- 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. 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.