Abstract
Genetics studies have identified the gene for the high-affinity IgE receptor (FcεRI) β subunit as a candidate gene for atopy. We have shown that β is an intrinsic signaling amplifier leading to enhanced allergic responses in vivo. Here we report that β has a second amplification function: the amplification of FcεRI cell surface expression. This function is due to an early association of β with α, resulting in improved trafficking and maturation of α and receptor complexes. These data provide a possible molecular explanation for the large difference in FcεRI density between β − cells such as monocytes, dendritic cells, and β + effector cells (mast cells, basophils). In β + cells, the combined signaling and expression amplification results in an estimated 12- to 30-fold amplification of downstream events.
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