EVIDENCE FOR A COMPLEMENT-MEDIATED INHIBITION AND AN ANTIBODY-DEPENDENT CELLULAR CYTOTOXICITY OF DERMAL FIBROBLASTS IN ALOPECIA-AREATA

Immunological mechanisms have long been suggested to mediate hair loss in alopecia areata. In this process hair bulb melanocytes and dermal papilla fibroblasts are believed to be primarily involved. In the pres ent study we further investigated the role of humoral factors in alope cia areata. Three different experiments were performed on normal human epidermal melanocytes as well as normal human dermal fibroblasts: (i) incubation with medium containing 2, 10, or 20% alopecia areata serum (n = 12 patients) for 16 h, (ii) incubation with medium supplemented with preheated alopecia areata serum (1 h at 56 degrees C) and healthy human fresh serum as a complement source (1:1) and (iii) incubation w ith 2, 10 or 20% alopecia areata serum but, in addition, containing pe ripheral blood mononuclear cells from healthy subjects (effector/targe t ratio, 50:1). As controls, normal human fibroblasts and normal human epidermal melanocyte cultures were also incubated with serum from hea lthy individuals (n = 5) under the same culture conditions. The result s showed that alopecia areata serum exerted a significant stimulation of proliferation of both normal human fibroblasts (p>0.05 at 2%, p>0.0 5 at 10%, p<0.05 at 20%), and normal human epidermal melanocytes (p>0. 05 at 2%, p<0.05 at 10%, p>0.05 at 20%). Interestingly, however, alope cia areata serum induced a significant dose-dependent proliferation in hibition of normal fibroblasts, when there were preheated and suppleme nted with a complement source (p<0.05 at 2%, p<0.05 at 10%, p<0.01 at 20%), and also when peripheral blood mononuclear cells were added (p<0 .05 at 2%, p<0.05 at 10%, p>0.05 at 20%). In both conditions, however, no significant influence was found after incubation of normal human e pidermal melanocytes with alopecia areata serum (p>0.05). Our data sug gest that dermal fibroblasts may somehow be involved in the pathogenes is of alopecia areata and that two mechanisms could possibly contribut e to their inhibition and damage: (1) a complement-mediated and (2) an antibody-dependent cellular cytotoxicity. The role of hair bulb melan ocytes remains to be further delineated.