Background: In previous studies, oral cyclosporine was highly effective in the treatment of patients with severe atopic dermatitis. In this study seven patients with severe and therapy-resistant atopic dermatitis underwent therapy with cyclosporine, 5 mg/kg/day, for 6 weeks.

Objective: The effect of cyclosporine on the expression of cytokines, which probably play a role in this disease, was examined.

Methods: The study was performed with a panel of antibodies as markers of inflammatory cells, adhesion molecules, and cytokines (interferon-γ [IFN-γ], tumor necrosis factor-α [TNF-α] and interleukins 1α, 1β, and 8 [IL-1α, IL-1β, and IL-8, respectively]). They were visualized by indirect immunoperoxidase techniques.

Results: After 2 weeks of cyclosporine therapy, a reduction of 60% in the disease (severity and extent) was observed. This reduction was 89% after 4 weeks and 90% after 6 weeks of therapy. Results of indirect immunoperoxidase stains performed on lesional skin sections after 2 weeks of treatment showed statistically significant reduced numbers of CD14⁺, CD25 (IL-2R⁺) and IL-8⁺ inflammatory cells in the dermis and CD36(OKM5)⁺ cells in both the epidermis and dermis. The number of cells expressing IFN-γ and TNF-α, assumed to be the products of the helper T-cell (TH)1 subset, was unaltered despite the impressive clinical benefit observed. Keratinocytes in lesional atopic skin did not express intercellular adhesion molecule type 1 (ICAM-1). The expression of the adhesion molecules ICAM-1, lymphocyte function-associated (LFA) type 1, and LFA-3 on inflammatory cells also remained unaffected by cyclosporine treatment.

Conclusion: A statistically significant reduction in the number of activated T cells and in the number of cells expressing the IL-2 receptor (CD25) paralleled a marked improvement in the disease and supports the view that atopic dermatitis is based on a T-cell-mediated immune inflammation.