Johns Hopkins University
Allergic disease is caused by the secretion of a variety of substances from basophils and mast cells which express the high affinity receptor for IgE, FceRI. These two cell types are exquisitely sensitive to stimulation, requiring only several hundred receptors for a moderate response. However, the typical cell of an atopic patient expresses one quarter million of these receptors. New therapeutic approaches to controlling this reaction depend on reducing IgE-mediated stimulation of these cells by reducing the amount of circulating IgE. It will be demonstrated that this approach only works because IgE itself regulates the expression of FceRI on these cells. The mechanism underlying this control by IgE remains unknown but characteristics of the regulation have suggested a process which is amenable to mathematical modeling. These characteristics will be discussed and a simple model will be presented which may explain some key features. Features of experimental regulation that are not well explained by the model will also be discussed.
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