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Application of Biochip Microfluidic Technology to Detect Serum Allergen-specific Immunoglobulin E sIgE
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CD23 provides a noninflammatory pathway for IgE-allergen complexes.

Paul Engeroff1, Flurin Caviezel1, David Mueller1

  • 1Department of Rheumatology, Immunology and Allergology, University Hospital Bern, Bern, Switzerland; Department of BioMedical Research, University of Bern, Bern, Switzerland.

The Journal of Allergy and Clinical Immunology
|August 23, 2019
PubMed
Summary

Free immunoglobulin E (IgE) triggers allergic inflammation via FcεRI, while IgE-allergen immune complexes (IgE-ICs) are noninflammatory, being cleared by CD23. This highlights distinct roles for IgE receptors in immune responses.

Keywords:
CD23FcεRIIgE clearanceIgE sensitizationIgE-allergen complexinflammation

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Area of Science:

  • Immunology
  • Allergy Research
  • Molecular Biology

Background:

  • Type I hypersensitivity involves allergen-specific immunoglobulin E (IgE) binding to the high-affinity FcεRI receptor on mast cells and basophils, leading to allergic inflammation.
  • CD23 (FcεRII), a low-affinity IgE receptor on B cells, regulates immune responses, with reciprocal allosteric inhibition observed upon simultaneous binding to IgE by FcεRI and CD23.
  • These interactions suggest distinct functional roles for FcεRI and CD23 in managing IgE.

Purpose of the Study:

  • To investigate how free IgE and IgE-allergen immune complexes (IgE-ICs) interact with the two IgE receptors, FcεRI and CD23.
  • To explore the functional consequences of these distinct binding pathways.

Main Methods:

  • In vitro binding and activation assays using human cells.
  • In vivo experiments assessing IgE pharmacokinetics and anaphylaxis in animal models.

Main Results:

  • FcεRI preferentially binds free IgE, whereas CD23 preferentially binds IgE-ICs.
  • Free IgE binding to FcεRI initiates allergic inflammation via effector cells.
  • IgE-ICs exhibit reduced FcεRI binding and enhanced CD23-dependent serum clearance, rendering them noninflammatory.

Conclusions:

  • IgE-ICs are noninflammatory due to decreased FcεRI engagement.
  • Increased targeting of the CD23 pathway by IgE-ICs facilitates their clearance.
  • This differential receptor engagement explains the distinct biological functions of free IgE and IgE-ICs.