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Cutting Edge: Death of a Dogma or Enforcing the Artificial: Monomeric IgE Binding May Initiate Mast Cell Response by Inducing Its Receptor Aggregation

Reinhard Schweitzer-Stenner^* and Israel Pecht^1,

^* Department of Chemistry, Drexel University, Philadelphia, PA 19104; and Department of Immunology, Weizmann Institute of Science, Rehovot, Israel

Several recent reports have suggested that binding monomeric IgE (mIgE) to its type 1 receptor, FcRI, on mast cells induces important responses. These observations contradict the notion that it is the aggregation of this receptor that is essential for initiating mast cell response. In the present study, we suggest that the most probable causes for the reported observations are the experimental protocol used combined with the high expression levels of the FcRI by mast cells. Specifically, we suggest using the published data and physicochemical calculations that the exceptionally high number of cell surface FcRI-bound monoclonal IgE yields, in the two-dimensions of the cells’ membranes, a situation where even a low affinity of these mIgE for epitopes on their own structure or on another cell surface component may lead to their aggregation. Hence, we hypothesize that the reported response to mIgE binding is a result of such an FcRI-IgE induced aggregation.

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