ArticleImmunology2005
Inhibition of immunoglobulin E synthesis through Fc gammaRII (CD32) by a mechanism independent of B-cell receptor co-cross-linking.
Article in Immunology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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
5 citing papers in PubMed, 14 citations in OpenAlex.
- BAFF and APRIL signaling in the B-cell lineage: implications for the pathogenesis of ANCA-associated vasculitis.Frontiers in immunology · 2026Review
- Genomic and transcriptomic analyses identify distinctive features of triple-negative inflammatory breast cancer.NPJ precision oncology · 2024Article
- Characterization of a membrane Fcγ receptor in largemouth bass (Micropterus saloumoides) and its response to bacterial challenge.Fish physiology and biochemistry · 2024Article
- Regulatory Role of Fc Receptor in mIgMFrontiers in immunology · 2021Article
- TLR9-mediated activation of dendritic cells by CD32 targeting for the generation of highly immunostimulatory vaccines.Human vaccines & immunotherapeutics · 2019Article
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
The inhibitory effect on antibody production by immune complexes has been shown to depend on co-ligation of the B-cell antigen receptor (BCR) with the low-affinity receptor for immunoglobulin G (IgG) (Fc gammaRIIb, CD32). Here we report that immunoglobulin E (IgE) synthesis, induced in a BCR-independent manner by interleukin-4 (IL-4) and anti-CD40 antibody, was inhibited by CD32 ligation. The observed effect was specific for CD32 as, first, antibodies directed against other B-cell surface structures had no inhibitory effect, and, second, treatment with anti-CD32 of cells that had been in culture for 2 days was ineffective owing to the down-regulation of CD32 expression. IgE inhibition was also observed in cells stimulated by IL-4/CD40 F(ab')(2) or IL-4 plus soluble CD40 ligand, demonstrating that co-cross-linking of CD32 and CD40 was not necessary to induce inhibition. Mechanistic studies into the IgE class switch process demonstrated that IL-4/anti-CD40-induced IgE germline gene transcription and B-cell proliferation were not affected by CD32 ligation. The data demonstrate that the negative regulatory role of the CD32 molecule is not restricted to BCR-induced B-cell activation, but is also functional on other B-cell activation pathways mediated by CD40 and IL-4.
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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.