Membrane-bound immunoglobulin E (mIgE) (mIgE)

The B-cell receptor (BCR) containing membrane-bound immunoglobulin E (mIgE) is a critical component of the allergic immune response, expressed on B cells that have class-switched to IgE but not yet become plasma cells [UniProt P01854]. Unlike secreted IgE, which triggers mast cell degranulation, mIgE acts as a signaling receptor that maintains the pool of IgE-producing cells and memory B cells [Brightling et al., 2015]. Therapeutic targeting of mIgE, primarily through monoclonal antibodies like quilizumab, aims to deplete these IgE-switched B cells via antibody-dependent cellular cytotoxicity (ADCC), thereby providing a disease-modifying approach by cutting off IgE production at the source [Gauvreau et al., 2014]. This strategy is distinct from neutralizing circulating IgE (e.g., with omalizumab) and is being investigated for long-term control of allergic asthma and chronic spontaneous urticaria [Harris et al., 2016]. Clinical challenges include the potential for increased susceptibility to helminth infections and the need for precise biomarkers to monitor the depletion of the IgE-switched B cell compartment. The M1-prime domain of mIgE provides a unique epitope for selective targeting, ensuring that secreted IgE is not affected and that the drug specifically hits the B-cell population [Chen et al., 2010]. Overall, the IgE BCR represents a high-value target for achieving durable remission in IgE-mediated diseases.

Other names

IgE B-cell receptormIgE-BCRMembrane IgEImmunoglobulin heavy constant epsilonIGHE

Depletion of IgE-switched B cells and memory B cells via antibody-dependent cellular cytotoxicity (ADCC) and neutralization of secreted IgE to prevent binding to high-affinity FcεRI receptors.