Mast cell stimulation by monoclonal antibodies specific for the Fcϵ receptor yields distinct responses of arachidonic acid and leukotriene C4 secretion

The release of arachidonic acid ([3H]AA) and leukotriene C4 (LTC4) from the rat mucosal mast cells of the RBL‐2H3 line stimulated by Fcϵ receptor‐specific monoclonal antibodies (mAb), by IgE and multivalent antigen, or by Ca2+ ionophores, was investigated. In parallel, secretion of the granular enzyme β‐hexosaminidase was also assayed. The release of [3H]AA and LTC4 in response to stimulation by three FcϵRI‐specific mAb shows similar quantitative differences to those observed for the secretion of granule‐stored mediators. The mAb F4 induced a substantial release of both [3H]AA and LTC4, which is as high as that induced by IgE and multivalent antigen. mAb J17 and H10 were found to induce an insignificant release of [3H]AA, but while J17 did induce release of LTC4, H10 failed to induce it, even though both J17 and H10 caused substantial release of β‐hexosaminidase. Ca2+ ionophores were found to be relatively more effective in inducing release of [3H]AA and LTC4 than in causing the secretion of granular mediators, as compared to cell stimulation by FcϵRI aggregation. These results illustrate that the cell responses of degranulation and de novo synthesis and release of mediators have different sensitivities to stimulation by (a) configurationally distinct FcϵRI dimers, (b) FcϵRI aggregates induced by IgE and multivalent antigen, and (c) Ca2+ ionophores.