Increased IL-12 Expression Found in Vitiligo
VIENNA — Interleukin-12 may play a pivotal role in the pathogenesis of vitiligo by promoting melanocyte destruction via cytotoxic immune responses, Marcel Brönimann, M.D., said at the annual meeting of the European Society for Dermatological Research.
Interleukin-12 is known to stimulate production of interferon-gamma and other type 1 cytokines and to activate cytotoxic T cells.
Interleukin-12 also generates Th1 cell-mediated immune responses, which are characteristic of many autoimmune dermatologic diseases, explained Dr. Brönimann of the University of Bern (Switzerland).
Armed with this knowledge about how interleukin-12 functions, Dr. Brönimann investigated interleukin-12 expression in vitiligo.
Dr. Brönimann used real-time polymerase chain reaction and immunohistochemical studies of punch biopsy specimens of lesional and nonlesional skin obtained from 23 patients with untreated vitiligo and 5 control subjects without vitiligo who were undergoing cosmetic plastic surgery.
Lesional skin contained significantly more interleukin-12 antibody-positive cells than did normal skin.
The interleukin-12 immunoreactivity was located chiefly in the cytoplasm of dermal macrophages and dendritic cells, and epidermal Langerhans cells.
The likely scenario is that dermal macrophages, dendritic cells, as well as epidermal Langerhans cells activate cytotoxic T cells by antigen presentation.
These findings provide further support for the hypothesis that vitiligo is an autoimmune disease, according to Dr. Brönimann, during his presentation at the meeting.