CHARACTERIZATION OF T-CELL SUBSETS INFILTRATING POSTBURN HYPERTROPHICSCAR TISSUES

In this study, skin-infiltrating cells were characterized in both the active and remission phases of post-burn hypertrophic scar biopsies. I mmunohistochemistry examination of active phase samples showed an abun dant presence of natural killer cells, T cells, macrophages, a low, pr esence of natural killer cells and the lack of B lymphocytes. lit acti ve hypertrophic scars T lymphocytes infiltrate deep into the superfici al dermis and are also observed in the epidermis: CD3+ cells were pres ent at about 222+/-107 per 0.25 mm(2). In particular the analysis of l ymphocyte subpopulations showed that CD4+ T cells predominate in the d ermis as well as in the epidermis of active hypertrophic scars whereas CD8+ cells were less well represented (CD4/CD8 ratio is 2.06). This d istribution was also shown in remission phase samples and in normotrop hic scar specimens, although the lymphocyte number uas significantly l ower. Approximately 70 per cent of T lymphocytes present in the tissue involved in active phase hypertrophic scar samples were activated (po sitive with anti-HLA-DR and IL-2 receptor antibodies) which is signifi cantly higher than remission phase hypertrophic and normotrophic scars , in which positivity was 40 and 38 per cent, respectively. Upon activ ation, the lesional lymphocytes release several cytokines, locally and transiently that interact with specific receptors in response to diff erent stimulation. Central to the immune hypothesis of hypertrophic sc ars is that some of the T-cell lymphokines act on keratinocytes, fibro blasts and other cell types to induce changes characteristic of these scars. The presence and close proximity of activated T lymphocytes and antigen-presenting cells of various phenotypes in both the epidermis and dermis of hypertrophic tissues provides strong circumstantial evid ence of a local immune response. However, the manner in which T cells achieve and maintain their activated state iii hypertrophic tissues is , not yet known, and both antigen-dependent and independent mechanisms may contribute. (C) 1997 Elsevier Science Ltd for ISBI All rights res erved.