COMPLEMENT ACTIVATION BY HIV-1-INFECTED TARGET-CELLS ENHANCES IL-2-STIMULATED BUT NOT UNSTIMULATED ADCC ACTIVITY MEDIATED BY PERIPHERAL-BLOOD MONONUCLEAR-CELLS

The goal of this study was to determine whether deposition of compleme nt C3 breakdown products on the surface of HIV-infected target cells c ould augment the levels of antibody-dependent cellular cytotoxicity (A DCC) mediated by peripheral blood mononuclear cells (PBMC). Although C 3 was deposited on the surface of infected cells in the presence of an ti-HIV antibody from infected persons, no increase in the levels of AD CC mediated by freshly isolated PBMC was seen with either infected H9 or CEM-NKr target cells. However, a significant increase in ADCC was o bserved due to deposition of C3 on target cells with IL-2-stimulated e ffector cells. These results show that C3 deposition on target cells c an increase ADCC cytotoxicity under certain conditions. Complement may thus contribute to destruction of HIV-infected cells through this mec hanism in vivo, although these experiments suggest that specific antib ody is the major targeting molecule for ADCC. (C) 1996 Academic Press Inc.