Incubation of rat lymphocytes with homologous IgE induced an increase in Fc epsilon R(+) lymphocytes and the formation of IgE-binding factors. Pretreatment of rat lymphocytes with 1 to 5 microM dexamethasone, however, prevented the IgE-induced expression of Fc epsilon R on both B and T lymphocytes. Upon incubation with IgE, T cells activated with 10 micrograms/ml Con A produced IgE-potentiating factors that had affinity for lentil lectin and selectively enhanced the IgE response. Pretreatment of the Con A-activated T cells with dexamethasone, before incubation with IgE, changed the nature of IgE-binding factors formed by the cells. The majority of IgE-binding factors formed by the dexamethasone-treated, Con A-activated cells failed to bind lentil lectin Sepharose and selectively suppressed the IgE response. An injection of 0.2 mg dexamethasone into rats infected with Nippostrongylus brasiliensis markedly diminished the proportion of Fc epsilon R(+) lymphocytes in their mesenteric lymph nodes. The lymph node cells from the infected animals spontaneously released IgE-potentiating factors in vitro. However, the majority of IgE-binding factors formed by the mesenteric lymph node cells from the dexamethasone-treated, Nb-infected animals lacked affinity for lentil lectin and selectively suppressed the IgE response. The results indicate that glucocorticoid treatment prevented the glycosylation of IgE-binding factors and thereby changed the biologic activities of the factors.