IgE/CD23-mediated transepithelial antigen transport in allergic intestines. In food allergy, Th2-skewing and IL-4 synthesis induce isotype switching in B cells to produce a large amount of IgE that is secreted into serum and gut lumen, or bound to high affinity receptor FcεRI on mast cell surface. IL-4 also acts on intestinal epithelial cells to upregulate the expression of low-affinity IgE receptor, CD23/FcεRII. Following exposure to dietary allergens, enhanced luminal-to-serosal transepithelial antigen transport is mediated by IgE/CD23 prior to mast cell activation during phase I. Transcytosed allergens reach the subepithelial lamina propria and cause IgE cross-linking on mast cells, resulting in cell degranulation and anaphylactic responses. The release of mast cell mediators, such as histamine, prostaglandin, serotonin and proteases, are known to induce epithelial ion secretion and to increase paracellular epithelial permeability in phase II.