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The Journal of Immunology, 2004, 172: 4048-4058.
Copyright © 2004 by The American Association of Immunologists

Monomeric IgE Stimulates NFAT Translocation Into the Nucleus, a Rise in Cytosol Ca2+, Degranulation, and Membrane Ruffling in the Cultured Rat Basophilic Leukemia-2H3 Mast Cell Line1

Vinita Pandey2, Shoji Mihara2, Amanda Fensome-Green, Stephen Bolsover and Shamshad Cockcroft3

Department of Physiology, University College London, London, United Kingdom

Mast cells are key regulators in allergy and inflammation, and release histamine, cytokines, and other proinflammatory mediators. In the classical view, IgE acts merely to prime mast cells, attaching to Fc{epsilon}Rs but not evoking any cell signaling response until cross-linked by the presence of a multivalent allergen. However, several recent studies have reported that IgE alone can promote cell survival and cytokine production in the absence of cross-linking by allergen. In this study we demonstrate that acute addition of monomeric IgE elicits a wide spectrum of responses in the rat basophilic leukemia-2H3 mast cell line, including activation of phospholipases C{gamma} and D, a rise in cytosol Ca2+, NFAT translocation, degranulation, and membrane ruffling within minutes. Calcium transients persist for hours as long as IgE is present resulting in the maintained translocation of the transcription factor NFAT to the nucleus. Removal of IgE reverses the signaling processes. Our results indicate that, far from simply preparing the cells for a response to allergen, monomeric IgE can stimulate signaling pathways that lead to degranulation, membrane ruffling, and NFAT translocation. The mechanism of activation is likely to be via aggregation of the Fc{epsilon}R1 because activation by IgE can be inhibited with monovalent hapten.




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