Abstract
IgE cross-linking is known to trigger inflammatory reactions to antigens after binding FcɛRI, a high-affinity IgE receptor present on mast cells or basophils. The second receptor engaged by IgE is the low-affinity IgE receptor, CD23/FcɛRII, most prominently expressed in B cells, which is thought to negatively regulate IgE levels. However, the mechanisms that regulate the targeting of the two receptors and the respective function of the two pathways in inflammation or homeostasis are not yet understood. We investigated several mechanisms related to the binding of IgE and antigen to both receptors, as well as the influence of such binding on different immune cells expressing the receptors. We showed that free IgE preferentially binds to FcɛRI whereas IgE immune complexes (IgE-ICs) are preferentially captured by CD23. Binding of IgE-ICs to CD23 on B cells can regulate serum IgE and prevent effector cell activation on one hand while on the other hand it can facilitate antigen presentation by delivering antigen to dendritic cells.
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