Evidence map›Paper›PMID 22393152›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2012

Soluble CD23 controls IgE synthesis and homeostasis in human B cells.

Alison M Cooper, Philip S Hobson, Mark R Jutton, Michael W Kao, Binia Drung, Boris Schmidt, David J Fear, Andrew J Beavil, James M McDonnell, Brian J Sutton and 1 more

Open access · greenAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
3.4field-weighted citation impact, top 7% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

38 citing papers in PubMed, 75 citations in OpenAlex.

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  9. Human IgE does not bind to human FcRn.Scientific reports · 2022
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 6 institutions in 2 countries.

Alison M CooperMedical Research Council and Asthma UK Centre in Allergic Mechanisms of Asthma, King's College London, Guy's Hospital, London SE1 9RT, UK.
Philip S Hobson
Mark R Jutton
Michael W Kao
Binia Drung
Boris Schmidt
David J Fear
Andrew J Beavil
James M McDonnell
Brian J Sutton
Hannah J Gould
Asthma UK · GBKing's College London · GBMedical Research Council · GBTechnical University of Darmstadt · DEGuy's Hospital · GBKing's College Hospital · GB

Funding

Department of HealthMedical Research Council G0400106Medical Research Council G0400503Medical Research Council G0400503(73410)Medical Research Council G0501494Medical Research Council G1000758Medical Research Council MR/J006742/1Wellcome Trust 076343
6 · The paper itself

Abstract

CD23, the low-affinity receptor for IgE, exists in membrane and soluble forms. Soluble CD23 (sCD23) fragments are released from membrane (m)CD23 by the endogenous metalloprotease a disintegrin and metalloprotease 10. When purified tonsil B cells are incubated with IL-4 and anti-CD40 to induce class switching to IgE in vitro, mCD23 is upregulated, and sCD23 accumulates in the medium prior to IgE synthesis. We have uncoupled the effects of mCD23 cleavage and accumulation of sCD23 on IgE synthesis in this system. We show that small interfering RNA inhibition of CD23 synthesis or inhibition of mCD23 cleavage by an a disintegrin and metalloprotease 10 inhibitor, GI254023X, suppresses IL-4 and anti-CD40-stimulated IgE synthesis. Addition of a recombinant trimeric sCD23 enhances IgE synthesis in this system. This occurs even when endogenous mCD23 is protected from cleavage by GI254023X, indicating that IgE synthesis is positively controlled by sCD23. We show that recombinant trimeric sCD23 binds to cells coexpressing mIgE and mCD21 and caps these proteins on the B cell membrane. Upregulation of IgE by sCD23 occurs after class-switch recombination, and its effects are isotype-specific. These results suggest that mIgE and mCD21 cooperate in the sCD23-mediated positive regulation of IgE synthesis on cells committed to IgE synthesis. Feedback regulation may occur when the concentration of secreted IgE becomes great enough to allow binding to mCD23, thus preventing further release of sCD23. We interpret these results with the aid of a model for the upregulation of IgE by sCD23.

Indexed as

Genes, ImmunoglobulinADAM10 ProteinADAM ProteinsAmyloid Precursor Protein SecretasesB-LymphocytesDipeptidesFeedback, PhysiologicalGene Expression RegulationHomeostasisHumansHydroxamic AcidsImmunoglobulin Class SwitchingImmunoglobulin EImmunologic CappingMembrane ProteinsProtease Inhibitors3-(formylhydroxyamino)-2-(3-phenyl-1-propyl)butanoic acid (2,2-dimethyl-1-methylcarbamoyl-1-propyl)amideADAM10 ProteinADAM10 protein, humanADAM ProteinsAmyloid Precursor Protein SecretasesDipeptidesHydroxamic AcidsImmunoglobulin EMembrane ProteinsProtease InhibitorsReceptors, Complement 3dReceptors, IgERecombinant Fusion ProteinsRNA, Small Interfering

Identifiers

PMID22393152
PMCPMC3378639
OpenAlexW2117284681

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.