Ultrastructural study of biochemically modulated ADCC in HSV-1 infected and uninfected Chang liver cells.
The effect of cytochalasin B, ouabain and 25-OH cholesterol on specific lysis due to antibody dependent cellular cytotoxicity (ADCC) in allogeneic and xenogeneic systems was studied using Herpes simplex I infected Chang liver cells. Cytochalasin B reduced both cytotoxicity and lymphocyte/target (LT) binding in the allogeneic system whereas cytotoxicity but not LT binding was reduced in the xenogeneic system. Ouabain inhibited ADCC in both systems as well as LT binding in the allogeneic system; however, binding in the xenogeneic system was not significantly reduced. The 25-OH cholesterol produced a marked decrease in ADCC in both systems but had no significant effect on LT binding in either system. The biochemical and ultrastructural data suggest that the modulators act at different stages in the ADCC response and that there may be more than one mechanism of ADCC to handle different types of target antigens.
D000818:Animals; D000920:Antibody-Dependent Cell Cytotoxicity / Q000187:drug effects*; D002460:Cell Line; D002462:Cell Membrane / Q000648:ultrastructure; D003571:Cytochalasin B / Q000494:pharmacology; D006888:Hydroxycholesterols / Q000494:pharmacology; D008099:Liver; D008214:Lymphocytes / Q000276:immunology / Q000648:ultrastructure; D008854:Microscopy, Electron; D008855:Microscopy, Electron, Scanning; D010042:Ouabain / Q000494:pharmacology; D018139:Simplexvirus / Q000276:immunology*
D006888:Hydroxycholesterols; D003571:Cytochalasin B; D010042:Ouabain; C007997:25-hydroxycholesterol