To characterize the defect responsible for abnormal histamine-induced suppressor cell function observed in atopic subjects, we studied histamine-induced suppressor factor (HSF) production and augmented prostaglandin E2 production. In addition, we exogenously provided interleukin 1 to determine whether abnormal histamine-induced suppressor cell function could be corrected by this monokine. Mononuclear cells from 16 asymptomatic atopic subjects generated significantly less (p less than 0.01) histamine-induced suppressor activity than cells from 10 nonatopic controls, and mean suppressor-factor production was also significantly reduced (p less than 0.01). The latter two responses were not corrected by interleukin 1. Atopic monocytes produced significantly less (p less than 0.01) prostaglandin E2 in response to suppressor factor than did control monocytes. The atopic group had phenotypically normal numbers of T-helper cells, T-suppressor cells, and ratios of these cells. These data indicate that despite having phenotypically adequate numbers, T-suppressor cells from atopics produce fewer suppressor signals than cells from nonatopics and their monocytes produce less prostaglandin E2 even if the suppressor signals are provided.