A model of IgE-induced adhesion to FN. IgE binding to the FcϵR1 on BMMCs allows them to aggregate at a low frequency. This results in a relatively low (compared with IgE + Ag) but prolonged signal that activates, among other pathways, the PI3K and PLCγ pathways. These 2 pathways play a critical role in IgE- and IgE + Ag-induced adhesion to FN by inducing the entry of extracellular calcium and the activation of a classical PKC. SF-induced adhesion of BMMCS to FN, however, appears to require the stimulation of the PI3K and PLCγ pathways and the subsequent critical activation of a novel (DAG-dependent, calcium-independent) PKC.