ArticleCurrent allergy and asthma reports2007
CD23: an overlooked regulator of allergic disease.
Article in Current allergy and asthma reports, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
50 citing papers in PubMed, 84 citations in OpenAlex.
- B cell-intrinsic Ssu72 phosphatase is a key regulator of allergic asthma.Experimental & molecular medicine · 2026Article
- Antibodies targeting a shared epitope exploit IgE allostery to drive distinct functional outcomes.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- The ADAM Family of Proteases: Structure, Substrates, and Roles in Liver Diseases.International journal of molecular sciences · 2026Review
- FcεRII (CD23) in dermatological disorders: structure, function, and clinical implications.Frontiers in allergy · 2026Review
- Intensity of CD23 expression on IgGThe journal of allergy and clinical immunology. Global · 2025Article
- Comparative Transcriptomic and Proteomic Analyses Identify Byssogenesis-Associated Genes in the Mediterranean MusselInternational journal of molecular sciences · 2025Article
- Vaccine-Induced Anti-IgE Antibodies Neutralize Free IgE but Fail to Bind and Activate Mast Cell-Displayed IgE.Allergy · 2025Article
- Review
- A Comparison of Natural and Therapeutic Anti-IgE Antibodies.Antibodies (Basel, Switzerland) · 2024Review
- On the complexity of IgE: The role of structural flexibility and glycosylation for binding its receptors.Frontiers in allergy · 2023Review
- 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
- Lack of Ecto-5'-Nucleotidase Protects Sensitized Mice against Allergen Challenge.Biomolecules · 2022Article
- Low-affinity but high-avidity interactions may offer an explanation for IgE-mediated allergen cross-reactivity.Allergy · 2021Article
- Reviving lost binding sites: Exploring calcium-binding site transitions between human and murine CD23.FEBS open bio · 2021Article
- Review
- Function of Protein S-Palmitoylation in Immunity and Immune-Related Diseases.Frontiers in immunology · 2021Review
- Immunoglobulins or Antibodies: IMGTBiomedicines · 2020Review
- Filling the Antibody Pipeline in Allergy: PIPE Cloning of IgE, IgGInternational journal of molecular sciences · 2020Article
- Article
- IgE Antibodies: From Structure to Function and Clinical Translation.Antibodies (Basel, Switzerland) · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Given the importance of immunoglobulin (Ig) E in mediating type I hypersensitivity, inhibiting IgE production would be a general way of controlling allergic disease. The low-affinity IgE receptor (FceRII or CD23) has long been proposed to be a natural regulator of IgE synthesis. In vivo research supporting this concept includes the observation that mice lacking CD23 have increased IgE production whereas mice overexpressing CD23 show strongly suppressed IgE responses. In addition, the finding that mice injected with monoclonal antibody directed against the coiled-coil stalk of CD23 have enhanced soluble CD23 release and increased IgE production demonstrates that full-length, trimeric CD23 is responsible for initiating an IgE inhibitory signal. The recent identification of ADAM10 (a disintegrin and metalloprotease) as the CD23 metalloprotease provides an alternative approach for designing therapies to combat allergic disease. Current data suggest that stabilizing cell-surface CD23 would be a natural means to decrease IgE synthesis and thus control type I hypersensitivity.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.