ArticleImmunity, inflammation and disease2015
High affinity targeting of CD23 inhibits IgE synthesis in human B cells.
Article in Immunity, inflammation and disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 33 citations in OpenAlex.
- FcεRII (CD23) in dermatological disorders: structure, function, and clinical implications.Frontiers in allergy · 2026Review
- Structural and Functional Insights Into IgE Receptor Interactions and Disruptive Inhibition.Immunological reviews · 2025Review
- The role of immunoglobulin E in non-atopic disorders.Frontiers in immunology · 2025Review
- Article
- Evaluation of Leukocytes, B and T Lymphocytes, and expression of CD200 and CD23 on B lymphocytes in Patients with Atopic Dermatitis on Dupilumab Therapy-Pilot Study.Dermatology and therapy · 2023Article
- On the complexity of IgE: The role of structural flexibility and glycosylation for binding its receptors.Frontiers in allergy · 2023Review
- Designed Ankyrin Repeat Proteins as a tool box for analyzing p63.Cell death and differentiation · 2022Article
- Immunomodulatory Effects of Mesenchymal Stem Cell-Derived Extracellular Vesicles in Allergic Airway Disease.Life (Basel, Switzerland) · 2022Review
- Review
- IgE-neutralizing UB-221 mAb, distinct from omalizumab and ligelizumab, exhibits CD23-mediated IgE downregulation and relieves urticaria symptoms.The Journal of clinical investigation · 2022Article
- The Potential of Exosomes in Allergy Immunotherapy.Vaccines · 2022Review
- IgE glycans promote anti-IgE IgG autoantibodies that facilitate IgE serum clearanceFrontiers in immunology · 2022Article
- Low-affinity but high-avidity interactions may offer an explanation for IgE-mediated allergen cross-reactivity.Allergy · 2021Article
- Review
- Past, present, and future of anti-IgE biologics.Allergy · 2020Review
- The mechanistic and functional profile of the therapeutic anti-IgE antibody ligelizumab differs from omalizumab.Nature communications · 2020Article
- The Intersection of IgE Autoantibodies and Eosinophilia in the Pathogenesis of Bullous Pemphigoid.Frontiers in immunology · 2019Review
- Article
- IgE binds asymmetrically to its B cell receptor CD23.Scientific reports · 2017Article
- Structural basis of omalizumab therapy and omalizumab-mediated IgE exchange.Nature communications · 2016Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The low-affinity IgE receptor FcϵRII (CD23) is part of the regulatory system controlling IgE synthesis in human B cells and exists in membrane and soluble forms. Binding of IgE to CD23 has been described to have stabilizing effects and to prevent cleavage of CD23. Previous experiments using anti-CD23 antibodies reduced IgE synthesis but were difficult to interpret as the antibody Fc part might also mediate feedback mechanisms. The purpose of this study was to investigate the regulatory role of CD23, by using designed ankyrin repeat proteins (DARPins) that specifically recognize CD23. Anti-CD23 DARPins were isolated by ribosome display and were produced as monovalent and bivalent constructs. Affinities to CD23 were measured by surface plasmon resonance. IgE synthesis and up-regulation of CD23 in human peripheral B cells were induced by IL-4 and anti-CD40 antibody. We assessed CD23 expression and its stabilization by FACS and used an ELISA for detecting soluble CD23. IgE synthesis was measured by ELISA and real-time PCR. Surface plasmon resonance revealed affinities of the DARPins to CD23 in the pico-molar range. Anti-CD23 DARPins strongly inhibited binding of IgE to CD23 and share thus a similar binding epitope as IgE. The DARPins stabilized membrane CD23 and reduced IgE synthesis in an isotype specific manner. Furthermore, the anti-CD23 DARPins decreased IgE transcript through inhibition of mature Cϵ RNA synthesis suggesting a posttranscriptional control mechanism. This study demonstrates that targeting CD23 alone is sufficient to inhibit IgE synthesis and suggests that a negative signaling occurs directly through the CD23 molecule.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.