Comparative Immunophenotypic Study of Lichen SclerosusEpidermotropic CD57plus; Lymphocytes Are Numerousmdash;Implications for Pathogenesis

摘要

To characterize the immunophenotype of inflammatory cells in lichen sclerosus (LS), we performed a comparative case control study using one-and two-color immunohistochemistry and the nitro blue tetrazolium (NBT) reaction. Study material consisted of 100 biopsies from patients with LS or from 12 control groups consisting of inflammatory, scarring, and depigmenting cutaneous disorders. In addition, fresh tissue was sampled from four vulvectomy specimens for NBT testing. The typical inflammatory infiltrate of LS contained numerous epidermotropic CD3plus;, CD8plus;, CD57plus; cells, increased intraepidermal HLA-DRplus; cells, and a dermal infiltrate rich in CD8plus;, CD57plus;, HLA-DRplus;, and CD68plus; inflammatory cells. Comparing LS to the 12 control groups, epidermotropic CD57plus; lymphocytes independently predicted LS (P equals; 0.006, logistic regression, multivariate analysis). Among the 12 control groups, only specimens of the inflammatory stage of morphea exhibited numerous dermal CD57plus; lymphocytes. Two-color immunohistochemistry confirmed the CD3plus;/CD8plus;CD57plus; and CD3plus;/CD8plus;/CD57plus;HLA-DRplus; epidermotropic and dermal lymphocytic phenotypes and the dermal macrophage CD68plus;HLA-DRplus; phenotype. In LS, the NBT reaction revealed evidence of superoxide production associated with CD68plus;HLA-DRplus; cells. Expansion of CD8plus;CD57plus; lymphocytes is associated with viral infections, autoimmune disease, malignancies, and transplantation and is suspected to be the result of chronic excessive antigen challenge. In these pathologic states, CD8plus;CD57plus; lymphocytes (as terminally differentiated, antigen-specific T cells) participate in the suppression of cytolytic activity to limit tissue damage. In LS, activated macrophages and lymphocytes indicate persistent antigen-driven inflammation. LS's numerous CD8plus;CD57plus; lymphocytes may be either the mediators or the consequence of its hallmark sclerosis.