Abstract

Background: The pathogenesis of lichen sclerosus (LS) and the mechanism of involution of LS-affected tissues is controversial. Autoimmune factors are proposed as a cause of disease. The involvement of autoimmune T lymphocytes in the disease development and progression is considered.Material/Methods: The investigation included 41 woman divided into two groups: a study group and controls. In the study group were 22 vulvular LS patients.Nineteen healthy woman underwent plastic surgery of the same area and served as controls. We analyzed reactive oxygen intermediate (ROI) production by peripheral blood granulocytes, the production of IL-2, IL-5, IL-10, IL-12, and TNF-a cytokines by lymphocytes, and the activation of CD25, CD26, CD69, CD71, and HLA DR antigen expression. Results: An increase in CD4+CD25+ suppressor T cells together with a decrease in CD3+CD26+ activated lymphocytes paralleled an increase in IL-10 production by peripheral blood lymphocytes of the lichen sclerosus patients. Diminished ROI production by peripheral blood granulocytes of LS patients was observed after both receptor-dependent and –independent stimulation. Baseline increase in IL-12 and stimulated increases in IL-2, IL-5, IL-10, and TNF-a production by lymphocytes of LS patients were also observed. Conclusions: The involution of lichen sclerosus-affected tissues may be the suppressive effect exerted by CD4+CD25+suppressor T lymphocytes, the increase in IL-10 inhibitory cytokine production, and diminished granulocyte ROI production. Infl ammatory infi ltrates in the affected regions of the skin are characterized by a diminished number of CD3 lymphocytes bearing the CD26 molecule, which may be responsible for an autocrine defect in bioactive mediator degradation.

Keywords: Lichen Sclerosus et Atrophicus - immunology, Adolescent, Autoimmune Diseases - pathology, CD4-Positive T-Lymphocytes - metabolism, Cytokines - metabolism, Leukocyte Count, Lichen Sclerosus et Atrophicus - pathology, Neutrophils - immunology, Reactive Oxygen Species - metabolism, Receptors, Interleukin-2 - metabolism, T-Lymphocytes - immunology