title: Biochemically damaged erythroblasts bind natural serum antibodies and activate complement.
abstract: Friend leukaemia erythroblasts which had been damaged biochemically by treatment with inhibitors of cellular metabolism (sodium fluoride, sodium azide) or of protein synthesis (cycloheximide, puromycin) were incubated with heat-inactivated or fresh mouse serum and tested for surface-bound IgG and C3c, respectively, by reaction with FITC-immunoconjugates followed by flow-cytofluorometry. Erythroblasts exposed to sodium azide, cycloheximide or puromycin showed specific binding of IgG; the extent of binding was related to the concentration of the drugs and duration of treatment. Moreover, prolonged exposure of the cells to the inhibitors of protein synthesis lead to a dose-dependent activation of complement. The results suggest that the opsonization of biochemically-damaged Friend leukaemia erythroblasts with IgG and C3 may facilitate their interaction with macrophages.
mesh_terms: D000888:Antibodies, Anti-Idiotypic / Q000276:immunology; D000937:Antigen-Antibody Reactions; D001386:Azides / Q000494:pharmacology; D002460:Cell Line; D003167:Complement Activation / Q000187:drug effects; D003513:Cycloheximide / Q000494:pharmacology; D004900:Erythroblasts / Q000187:drug effects / Q000276:immunology*; D005622:Friend murine leukemia virus; D006801:Humans; D007074:Immunoglobulin G / Q000276:immunology*; D004915:Leukemia, Erythroblastic, Acute / Q000276:immunology; D007942:Leukemia, Experimental / Q000276:immunology; D011691:Puromycin / Q000494:pharmacology; D019810:Sodium Azide; D012969:Sodium Fluoride / Q000494:pharmacology
chemical_list: D000888:Antibodies, Anti-Idiotypic; D001386:Azides; D007074:Immunoglobulin G; D011691:Puromycin; D012969:Sodium Fluoride; D019810:Sodium Azide; D003513:Cycloheximide