In the presence of decomplemented sera from 13 out of 14 patients with Hashimoto's disease and 6 out of 7 patients with Graves' disease, normal human leucocytes caused significant lysis of cultured thyroid cells, as estimated by the release of (51)Cr. Cytolysis was seen to proceed linearly during the first 9 hours, but ceased after that. Cytolysis was enhanced by the addition of complement at as low as the concentration which did not induce cytotoxic factor mediated lysis. A study of different effector cells mediating ADCC indicated that mononuclear and non-adherent cells were cytotoxic to cultured thyroid cells, but adherent cells were not effective in this system. The percentage of cytotoxicity correlated with the anti-microsomal antibody(MCHA) titer (r=0.63, p<0.01), but not with the anti-thyroglobulin antibody (TGHA) titer. Inhibition of ADCC by aggregated IgG suggested that immune complexes in the sera of patients with thyroid disorders might inhibit cell destruction by an ADCC mechanism.