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* Division of Cell Biology, La Jolla Institute for Allergy and Immunology, San Diego, CA 92121;
Division of Vascular Biology, Department of Cell Biology, Scripps Research Institute, La Jolla, CA 92037;
Max Planck Institute for Experimental Endocrinology, Hannover, Germany; and
Department of Laboratory Medicine, University of California, San Francisco, CA 94143-0134
Mast cells play a critical role in IgE-dependent immediate hypersensitivity. Recent studies have shown that, contrary to the traditional view, binding of monomeric IgE to Fc
RI results in a number of biological outcomes in mast cells, including survival. However, IgE molecules display heterogeneity in inducing cytokine production; highly cytokinergic (HC) IgEs cause extensive FcRI aggregation, which leads to potent enhancement of survival and other activation events, whereas poorly cytokinergic (PC) IgEs can do so inefficiently. The present study demonstrates that HC, but not PC, IgEs can efficiently induce adhesion and spreading of mouse mast cells on fibronectin-coated plates in slow and sustained kinetics. HC IgE-induced adhesion through 
1 and 7 integrins promotes survival, IL-6 production, and DNA synthesis. Importantly, we have identified Lyn and Syk as requisite tyrosine kinases and Hck, Btk, and protein kinase C 
as contributory kinases in HC IgE-induced adhesion and spreading, whereas protein kinase C plays a negative role. Consistent with these results, Lyn, Syk, and Btk are activated in HC IgE-stimulated cells in a slower but more sustained manner, compared with cells stimulated with IgE and Ag. Thus, binding of HC IgEs to FcRI induces adhesion of mast cells to fibronectin by modulating cellular activation signals in a unique fashion.
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