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Complement activation by HIV-1-infected target cells enhances IL-2-stimulated but not unstimulated ADCC activity

I Sereti1, G T Spear

  • 1Department of Immunology/Microbiology, Rush Medical School, Chicago, Illinois 60612, USA.

The goal of this study was to determine whether deposition of complement C3 breakdown products on the surface of HIV-infected target cells could augment the levels of antibody-dependent cellular cytotoxicity (ADCC) mediated by peripheral blood mononuclear cells (PBMC). Although C3 was deposited on the surface of infected cells in the presence of anti-HIV antibody from infected persons, no increase in the levels of ADCC mediated by freshly isolated PBMC was seen with either infected H9 or CEM-NKr target cells. However, a significant increase in ADCC was observed due to deposition of C3 on target cells with IL-2-stimulated effector cells. These results show that C3 deposition on target cells can increase ADCC cytotoxicity under certain conditions. Complement may thus contribute to destruction of HIV-infected cells through this mechanism in vivo, although these experiments suggest that specific antibody is the major targeting molecule for ADCC.

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