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RI
-ITAM Is Differentially Required for Mast Cell Function In Vivo1
Departments of
*
Molecular Genetics and
Otorhinolaryngology, Graduate School of Medicine, Chiba University, Chiba, Japan;
PRESTO, Japan Science and Technology, Kawaguchi, Japan; and
Laboratory for Cell Signaling, RIKEN Research Center for Allergy and Immunology, Yokohama, Japan
The cross-linking of IgE-bound Fc
RI by Ags triggers mast cell activation leading to allergic reactions. The in vivo contribution of FcRI
signaling to IgE/FcRI-mediated mast cell responses has not yet been elucidated. In this study FcRI-/- mast cells were reconstituted with either wild-type or mutant FcRI in transgenic mice and transfected mast cells in vitro. We demonstrate that FcRI-immunoreceptor tyrosine-based activation motif is essential for degranulation, cytokine production, and PG synthesis as well as for passive systemic anaphylaxis. Recent reports have suggested that cell surface FcRI expression and mast cell survival are regulated by IgE in the absence of Ag, although the molecular mechanism is largely unknown. We also found that the promotion of mast cell survival by IgE without Ags is mediated by signals through the FcRI-immunoreceptor tyrosine-based activation motif. In contrast, the IgE-mediated up-regulation of FcRI is independent of FcRI signaling. These results indicate that FcRI-mediated signals differentially regulate the receptor expression, activation, and survival of mast cells and systemic anaphylaxis.
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