Evidence for the involvement of cellular immunity in the etiopathogenesis of the hypopigmentary disorder vitiligo is provided by rare cases of inflammatory vitiligo. Nonlesional, perilesional, and lesional skin biopsies from three inflammatory vitiligo patients were immunohistochemically analyzed. The composition of inflammatory infiltrates present in perilesional skin was analyzed by antibodies to T cells (CD2, CD3, CD4, and CD8), Langerhans cells (CD1a), and macrophages (CD36 and CD68). The presence of activation markers on inflammatory cells was evaluated by analysts of HLA- DR, interleukin-2 receptor, and HECA-452 expression. The presence or absence of melanocytes was determined by the antibody NKI-beteb. Moreover, the abundance of matrix molecule tenascin was semiquantified using T2H5. Results indicate that within perilesional skin epidermis-infiltrating T cells exhibit an increased CD8/CD4 ratio and increased cutaneous lymphocyte antigen and interleukin-2 receptor expression. These cells are frequently juxtapositionally apposed to remaining melanocytes. In perilesional dermis, CD68 +OKM5 - macrophages were more numerous than in lesional or nonlesional skin. Keratinocytes as well as melanocytes consistently express major histocompatibility complex class H antigens along stretches of basal and suprabasal layers in perilesional epidermis. Moreover, inflammation is accompanied by increased tenascin content. Although these observations do not permit differentiation between the immune infiltrates being a result as opposed to the cause of the disease process, results presented in this study are very suggestive of involvement of local immune reactivity in melanocyte destruction.
|Original language||English (US)|
|Number of pages||10|
|Journal||American Journal of Pathology|
|State||Published - Apr 1 1996|
ASJC Scopus subject areas
- Pathology and Forensic Medicine