Relative contributions of decay accelerating factor (DAF), membrane cofactor protein (MCP) and CD59 in the protection of melanocytes from homologous complement.

Complement regulatory molecules, membrane cofactor protein (MCP), decay accelerating factor (DAF) and CD59, protect body cells from autologous complement. They have wide tissue distribution but nothing is known about the expression of these molecules on human melanocytes. Since melanocytes are lysed in the lesional skin of patients with a depigmentary disorder vitiligo, it is important to compare the protection offered by complement regulatory molecules to melanocytes present in normal and vitiligo epidermis, against autologous complement. From this point of view, we investigated the differential expression of MCP, DAF and CD59 on normal cultured human melanocytes and assessed their individual contribution in the protection of these cells against complement-mediated damage. Flow cytometric analysis showed that MCP and DAF but not CD59 were expressed on cultured melanocytes. When heat inactivated sera of patients with vitiligo were used as a source of anti-melanocyte antibody to sensitize melanocytes, and guinea pig serum (GpS) or normal human serum (NHS) as a source of complement, GpS was found to be more effective in causing the lysis of melanocytes than NHS. When melanocytes were sensitized with autoantibody as well as F(ab')2 fragment of either anti-MCP or anti-DAF and subsequently incubated with NHS or GpS, both antibody fragments increased the killing of melanocytes by NHS as well as by GpS. F(ab')2 fragment of anti-DAF was much more effective in causing enhancement of lysis than that of anti-MCP. Thus, cultured normal human melanocytes express functionally active MCP and DAF but not CD59. Contribution of DAF in protecting melanocytes against complement attack was much more than that of MCP.