Experiments were designed to investigate whether glucocorticoid-mediated immunosuppression are involved in glucocorticoid receptor activation. It was shown that RU486, a blocker of glucocorticoid, reversed dexamethasone (DEX)-mediated suppression of CD25 antigen expressions on ConA-stimulated lymphocytes, as determined with anti-CD25 monoclonal antibody. By means of radioligand binding assay, changes in high affinity IL-2 receptor were examined. The data indicated that RU486 alone was unable to affect high affinity IL-2 receptor expressions, but antagonized DEX-mediated down regulation of high affinity IL-2 receptor on cellular surface. The maximal binding capacities of IL-receptor were 10.0 +/- 0.7, 10.4 +/- 2.1, 6.5 +/- 0.8 and 12.1 +/- 2.7 fmol/10(7) cell respectively in four groups of the normal, RU486, DEX, and DEX plus RU486. The results suggest that such effects of DEX may be mediated through glucocorticoid receptor in lymphocytes.