Target intelligence / Profile preview

Membrane-bound immunoglobulin E receptor (mIgE)

Target
mIgE
Molecular classification
Immunoglobulin, B cell antigen receptor (IgE isotype), Receptor
01

Overview

Membrane-bound immunoglobulin E (mIgE) is the isoform of IgE expressed on the surface of B cells as part of the B cell antigen receptor (BCR) complex after class switch recombination to the epsilon (ε) heavy chain. This membrane form serves as the antigen-specific receptor that allows B cells to recognize allergens and respond by activating and ultimately differentiating into IgE-secreting plasma cells. In humans, mIgE can exist in multiple isoforms generated by alternative splicing, including a variant with an extracellular membrane-proximal domain that restricts surface expression and B cell activation[1][2]. mIgE+ B cells are rare in vivo and have a short lifespan, functioning mainly as transient precursors to plasma cells[2]. Interactions between mIgE and accessory molecules such as CD23 on B cells are crucial for regulating IgE synthesis and homeostasis, with implications in the pathogenesis and therapy of allergic diseases[5][6].\n\nKey points:\n- mIgE is not to be confused with secreted IgE (the antibody in plasma); mIgE acts as a B cell receptor before secretion[3][4].\n- Targeting mIgE directly is a potential but challenging strategy in allergy therapy due to safety concerns regarding unwanted immune activation[1].\n- Omalizumab and related anti-IgE antibodies primarily target circulating IgE, indirectly reducing mIgE+ B cells but do not bind membrane-bound IgE to avoid triggering degranulation[1].

Other names
Membrane IgEmIgE receptorB cell antigen receptor IgE isotypesurface IgEIgE-BCR
02

Mechanism of action

Inhibition of IgE binding to high-affinity FcεRI receptors on mast cells (by lowering available IgE); Reduction of IgE-expressing B cell survival by depleting free IgE (indirect effect).

03

Biological functions

Antigen recognitionB cell activationImmune responseRegulation of IgE production
04

Disease associations

AllergyInflammationHypersensitivity reactionsOther IgE-mediated diseases
05

Safety considerations

Risk of anaphylaxis if mIgE is directly targeted by therapeutic antibodies, due to rapid mast cell/basophil activationDifficulties in selectively depleting IgE+ B cells without affecting other immunoglobulin isotypes
06

Interacting drugs

Omalizumab (indirect; targets free IgE, thereby reducing mIgE-expressing B cells)

1 more in the full profile.

07

Biomarkers

Surface mIgE expression for identifying IgE-switched B cellsSerum IgE levels as markers of allergy risk and Th2 inflammation

Beyond the preview

Go deeper on Membrane-bound immunoglobulin E receptor (mIgE).

Explore the evidence, development activity, and competitive landscape with Gosset’s full data platform.

Drug pipeline

Full profile access

Explore the programs pursuing this target and their development progress.

  • Drug candidates
  • Developers
  • Development stage

Clinical trials

Full profile access

Follow the clinical studies evaluating therapies directed at this target.

  • Trial design
  • Status
  • Readouts

Competitive landscape

Full profile access

Compare approaches across drug candidates, modalities, and indications.

  • Programs
  • Modalities
  • Indications

Literature & evidence

Full profile access

Investigate the research and source evidence behind target biology and development.

  • Publications
  • Sources
  • Analysis

Patents

Full profile access

Explore patent activity around therapies and technologies addressing this target.

  • Patents
  • Assignees
  • Technologies

Research & analysis

Full profile access

Connect target biology, drug development, and emerging evidence in your research.

  • Biology
  • Development news
  • Analysis

Bring the full picture into focus.

See how Gosset can support your research on Membrane-bound immunoglobulin E receptor (mIgE).

Explore the full profile

Gosset Free

Get started with Gosset.

Enter your work email and we’ll be in touch with next steps.

Work email preferred.

Book a call