The relationship between glucocorticoid effect and regulation of cell surface antigens was investigated in two models of leukemic cell lines, CEM C7 denoted (r+, ly+) and CEM C1 (r+, ly-). The reactivity of murine monoclonal antibodies, anti-CD4-FITC, anti-CD8-FITC, anti-CD2-FITC and anti-calla-FITC, were analyzed using flow cytometry. The suppressor function was determined using [3H]thymidine incorporation into phytohemagglutinin-activated peripheral blood lymphocytes. Dexamethasone treatment of a human leukemic cell clone CEM C7 caused an increase in a subset of cells expressing the surface antigen CD8, which is present on suppressor and cytotoxic T-lymphocytes. By comparison, there was no modification of the expression of CD4 antigen, which is expressed at high levels in these cells. After two days of treatment with 5 x 10(-8) M dexamethasone, CEM C7 cells showed a two-fold increase in suppressor activity compared to untreated cells. In contrast, there was no regulation by glucocorticoids of either the CD8 or CD4 antigens in the leukemic clone CEM C1. Furthermore, no modification of the suppressor function in CEM C1 cells by dexamethasone was observed. In the human leukemic cells studied here, the ability to induce CD8 antigen expression in a CD4+ cells correlates with the ability to induce cell lysis in a glucocorticoid receptor positive cell population.