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 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.
Sereti
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I
Department of Immunology/Microbiology, Rush Medical School, Chicago, Illinois 60612, USA.
Spear
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GT
D000920:Antibody-Dependent Cell Cytotoxicity / Q000187:drug effects; D002460:Cell Line; D003167:Complement Activation / Q000187:drug effects / Q000502:physiology*; D003601:Cytotoxicity Tests, Immunologic; D015658:HIV Infections / Q000276:immunology*; D015497:HIV-1 / Q000276:immunology*; D006801:Humans; D007376:Interleukin-2 / Q000494:pharmacology*; D007963:Leukocytes, Mononuclear / Q000187:drug effects / Q000378:metabolism* / Q000821:virology*; D008213:Lymphocyte Activation
D007376:Interleukin-2