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Normal mouse mast cells (MCs) produced and released tumor necrosis factor-alpha (TNF-alpha) and had phagocytosis activity when stimulated by the calcium ionophore A23187, when accompanied by the changes of the morphology and Fc epsilon RI expression. Prior stimulation of MCs enhanced the superantigen Staphylococcus aureus enterotoxin B (SEB)-mediated TNF-alpha production in MC cultures. Although no increase in the release of TNF-alpha was observed when MCs were co-cultured with mitomycin C (MMC)-treated splenic adherent cells, the SEB-mediated TNF-alpha release was increased. Furthermore, the increase of TNF-alpha production was observed only when MCs were co-cultured with non-irradiated splenic adherent cells. There were some additional differences of the effects of irradiation on the MC-splenic adherent cell co-cultures. When irradiated MCs were co-cultured with splenic adherent cells the TNF-alpha production was increased to about the same level as that of the non-irradiated MCs in the co-cultures. Furthermore, the release of IgE was enhanced in the co-cultures of MCs with irradiated splenic adherent cells, but not in those of non-irradiated splenic adherent cells. However, the expression of Fc epsilon RI on the surface of MCs was significantly enhanced in both co-cultures. The increased expression of Fc epsilon RI on MCs in the co-cultures was suppressed by the addition of mitomycin C, ethylenediaminetetraacetic acid, dithiothreitol, diethyl maleate, or N-acetyl-L-cysteine. The present study revealed that, if the signals are transmitted via Fc epsilon RI from the splenic adherent cells, the