Langerhans cells (LCs) subserve an important antigen-presenting function in the skin immune system. They bear CD4 receptors, which make them potential targets for infection with the human immunodeficiency virus (H1V-1). The observation of reduced numbers of LCs in the skin of patients with the acquired immunodeficiency syndrome (AIDS), and the association of severe psoriasis with HIV-1 infection, raise interesting questions regar;iing the role of LCs in the skin of HIV-1-positive psoriatic patients. In this study, LCs were quantified in the lesional and non-lesional skin of seven HIV-1-positive psoriatic patients, and the results were compared with age-, sex- and site-matched HIV-l-negative psoriatic patients. The number of LCs was determined by staining skin sections with S-100 polyclonal antibody, using the three-step avidin-biotin immunoperoxidase method. The S-100-positive cells above the basal layer were quantified in two ways: cells/mm(2) of epidermal area, and cells/mm of length of basement membrane. HIV-l-positive psoriatic patients showed a reduction in the number of epidermal LCs compared with HIV-l-negative psoriatic patients using both methods of quantification, in both lesional and nonlesional skin (P < 0.05, Mann-Whitney test). In addition, a reduction in the number of LCs in lesional compared with non-lesional skin was observed in both HIV-1-positive and -negative patients when LCs were quantified per mm(2) of epidermal area (P < 0.05, Wilcoxon test). This reduction was also observed when LCs were quantified per mm length of basement membrane, but the reduction was not statistically significant in the control group of HIV-1-negative psoriatic patients. Our findings of a reduced number of LCs in the epidermis of HIV-1-positive psoriatic patients may be associated with the clinical deterioration of psoriasis in these patients.
