Evidence map›Paper›PMID 19494337›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2009

Suppression of IgE B cells and IgE binding to Fc(epsilon)RI by gene therapy with single-chain anti-IgE.

Takayuki Ota, Miyo Aoki-Ota, Bao Hoa Duong, David Nemazee

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.7field-weighted citation impact, top 32% 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

13 citing papers in PubMed, 23 citations in OpenAlex.

  1. Trial
  2. Single-Domain Antibodies-Novel Tools to Study and Treat Allergies.International journal of molecular sciences · 2024
    Review
  3. Flow Cytometric Identification of Human IgEMethods in molecular biology (Clifton, N.J.) · 2024
    Article
  4. B cell receptor ligation induces IgE plasma cell elimination.The Journal of experimental medicine · 2023
    Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
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

4 authors at 1 institution in 1 country.

Takayuki OtaDepartment of Immunology and Microbial Science, The Scripps Research Institute, La Jolla, CA 92037, USA.
Miyo Aoki-Ota
Bao Hoa Duong
David Nemazee
Scripps Research Institute · US

Funding

Immune Tolerance in Non-Clonal Immune SystemsR01AI059714 · NIAID · SCRIPPS RESEARCH INSTITUTE, THE · PI NEMAZEE, DAVID · 2004 to 2013
$3.9M
Manipulating the IgE response with IgE-reactive macroself antigenR21AI069866 · NIAID · SCRIPPS RESEARCH INSTITUTE, THE · PI NEMAZEE, DAVID · 2006 to 2007
$412k
NIAID NIH HHS R01 AI059714NIAID NIH HHS R21 AI069866NIAID NIH HHS R21AI069866
6 · The paper itself

Abstract

IgE plays a pivotal role in allergic reactions and asthma through its ability to bind to the mast cell FcR for IgE (FcepsilonRI). Current therapies to suppress such reactions include passive treatment with neutralizing Abs to IgE that block its binding to FcepsilonRI. In theory, induction of immune tolerance in the B lymphocytes that carry IgE Ag receptors and give rise to IgE-secreting cells should provide longer term efficacy. However, recent data have suggested that such memory cells may lack cell surface IgE. Using a gene therapy approach, we show that a recombinant single-chain neutralizing anti-IgE could not only neutralize circulating IgE, but also reduce IgE(+) B cell numbers and H chain transcripts. Therapeutic anti-IgE stimulated a calcium response in primary B cells or in a B cell line expressing membrane IgE and suppressed IgE secretion in vitro, suggesting that active signaling through membrane IgE likely promoted tolerance. Interestingly, upon subsequent challenge of anti-IgE-treated mice with an IgE cross-linking reagent capable of inducing activation of IgE-decorated mast cells, an anaphylaxis reaction was induced, apparently via a FcgammaRIII pathway involving recognition of anti-IgE Ab itself. These studies have important implications for the optimal design of safe and effective anti-IgE therapies and suggest that the IgE memory B cells may be targeted by such genetic Ab therapies.

Indexed as

Genetic TherapyAnaphylaxisAnimalsB-LymphocytesCell LineHumansImmunizationImmunoglobulin EMiceMice, Inbred BALB CProtein BindingReceptors, IgERecombinant ProteinsImmunoglobulin EReceptors, IgERecombinant Proteins

Identifiers

PMID19494337
PMCPMC2874974
OpenAlexW1957595469

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.