Monomeric IgE stimulates signaling pathways in mast cells that lead to cytokine production and cell survival

Although IgE binding to mast cells is thought to be a passive presensitizat ion step, we demonstrate herein that monomeric IgE (mIgE) in the absence of antigen (Ag) stimulates multiple phosphorylation events in normal murine b one marrow-derived mast cells (BMMCs). While mIgE does not induce degranula tion or leukotriene synthesis, it leads to a more potent production of cyto kines than IgE + Ag. Moreover, mIgE prevents the apoptosis of cytokine-depr ived BMMCs, likely by maintaining Bcl-X-L levels and producing autocrine-ac ting cytokines. The addition of Ag does not increase this IgE-induced survi val. Since IgE concentrations as low as 0.1 mug/ml enhance BMMC survival, e levated plasma IgE levels in humans with atopic disorders may contribute to the elevated mast cell numbers seen in these individuals.