Abstract
Dysregulation of the skin immune system (SIS) could explain the high prevalence of skin disorders in HIV+ individuals. The present study was carried out to determine whether alterations in the cell population of SIS and epidermal immunoactivation occur in the normal skin of HIV+ individuals. Forty-five biopsies were taken from the normal upper arm skin of 45 HIV+ patients and of 15 healthy controls. HIV+ individuals were divided into three categories according to their CD4 cell blood count (<200, 200-499 and > or = 500/microl). Hematoxylin-eosin was used to stain tissue sections for morphological analysis and immunohistochemistry was used for the evaluation of the frequency of macrophages, Langerhans cells, and CD lymphocyte subsets. In addition, semiquantitative analysis of LFA-1, ICAM-1 and HLA-DR was determined in epidermal cells. Macrophages, Langerhans cells, and CD lymphocyte subsets did not differ significantly between any of the patient categories and the control group. When all HIV+ individuals were compared as a group to the control group, a significant increase in dermal CD8+ T lymphocytes (P < 0.01) and lower CD4-CD8 ratios (P < 0.01) were observed in the HIV+ individuals. Epidermal ICAM-1 and HLA-DR expression was negative in both HIV+ and normal skin biopsies. No evidence of a depletion of the SIS population or of epidermal immunoactivation in normal skin from HIV+ individuals was demonstrable, suggesting that alterations in the central immune system are not necessarily reflected in the SIS of HIV-infected patients.
Highlights
During HIV infection, the skin is an organ of major morbidity
A significant increase in CD8 T lymphocytes was detected in HIV+ individuals (5.3 ± 7.3) in the perivascular dermis compared to control (0.6 ± 1; P < 0.01)
A positive correlation was observed between the number of CD3 and CD8 T lymphocytes (r = 0.29; P < 0.028) and between the number of CD4 lymphocytes and the CD4-CD8 ratio in the perivascular dermis (r = 0.80; P < 0.001) in all individuals
Summary
Severe cutaneous disorders most commonly occur during the course of the disease and sometimes they provide the earliest clue to the existence of HIV or of its progression [1,2,3]. Suggestive of both local permissiveness and responsiveness to the presence of HIV, a change in the cutaneous environment appears to take place. Most of the studies on SIS in HIV infection have focused on the role of Langerhans cells (Lc), most probably because of their important function as antigen-presenting cells and because of their expression of CD4 cells. As can be seen in a wide variety of dermatoses, keratinocytes may become immunoactivated by means of the induction of expression molecules, such as the intercellular adhesion molecule 1 (ICAM-1) and human leukocyte antigen (HLA)-DR, responsible for the increase in lymphocyte traffic in the epidermis and its susceptibility to inflammatory reactions [19]
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