Biochemically damaged erythroblasts bind natural serum antibodies and activate complement.
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.
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
D000888:Antibodies, Anti-Idiotypic; D001386:Azides; D007074:Immunoglobulin G; D011691:Puromycin; D012969:Sodium Fluoride; D019810:Sodium Azide; D003513:Cycloheximide