Rat eosinophil-mediated antibody-dependent cellular cytotoxicity: investigations of the mechanisms of target cell lysis and inhibition by glucocorticoids.

Purified eosinophils from the peritoneal washings of N. brasiliensis infected rats demonstrated antibody-dependent cellular cytotoxicity (ADCC) for 51Cr-labelled chicken erythrocytes. The F(ab')2 fragment of the antibody did not support cytotoxicity thereby demonstrating the importance of the eosinophil Fc receptor to this activity. Bystander lysis of erythrocytes did not occur, indicating that the eosinophil does not release lytic agents free into the medium. Cytochalasin B (1.25-5 micrograms/ml) colchicine (10(-5)-10(-3) M) and chloroquine (10(-4)-10(-3) M) inhibited eosinophil ADCC. Inhibition was also demonstrated by methylprednisolone, 10(-7)-10(-3) M and this inhibition was blocked by the protein synthesis inhibitor, cycloheximide (25 micrograms/ml). Cycloheximide alone had no effect. This block of steroid inhibition by cycloheximide suggests that the steroid effect on this system may be mediated by a newly synthesized protein and implies that the eosinophil may possess a glucocorticoid receptor.