Glucocorticoid hormones have been identified as one of the B cell activating signals necessary in IgE synthesis in the presence interleukin 4(IL-4). One question to be addressed in IgE synthesis is whether there is difference between atopics and non-atopics. In the present study, we aimed at looking the different effects of interleukin 4(IL-4) and hydrocortisone(HC) in IgE synthesis by peripheral blood monounclear cells (PBMCs) from 12 atopic patients and 6 non-atopic controls. PBMCs were cultured with IL-4 and/or HC for 14 days, and net IgE production was measured in the supernatant. Significant spontaneous IgE production by PBMCs was oberserved only in atopics. IL-4 increased net IgE synthesis by PBMCs from both atopics and non-atopics by similar amounts, whereas HC had that effect only in some atopics who showed high spontaneous IgE production. HC acted synergically with IL-4 in a narrow range of concentration which is individually different. This effect was more remarkable in subjects with low total serum IgE levels. These data suggest that atopic patients may have larger numbers of B cells committed to produce IgE, and that the effect of HC on IgE synthesis in vitro may be due to the priming effect of IL-4 in vivo.