Evidence map›Paper›PMID 33999439›Full record

ReviewAllergy2021

The role of allergen-specific IgE, IgG and IgA in allergic disease.

Mohamed H Shamji, Rudolf Valenta, Theodore Jardetzky, Valerie Verhasselt, Stephen R Durham, Peter A Würtzen, R J Joost van Neerven

Open access · hybridAbstract readReview
In one paragraph

Review in Allergy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 144 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
144citing papers in PubMed, 1 pooled it
25.1field-weighted citation impact, top 1% 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

144 citing papers in PubMed, 1 synthesis or guideline pooled it, 305 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Trial
  5. Trial
  6. Trial
  7. Trial
  8. Trial
  9. Observational
  10. Article
  11. Recent advances in allergen immunotherapy.Chinese medical journal · 2026
    Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Review
  19. A longitudinalScientific data · 2026
    Article
  20. Article

84 more citing papers are in PubMed but not listed here.

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

7 authors at 6 institutions in 7 countries.

Mohamed H ShamjiImperial College London, National Heart & Lung Institute, London, UK.ORCID 0000-0003-3425-3463
Rudolf ValentaDepartment of Pathophysiology and Allergy Research, Medical University of Vienna, Vienna, Austria.ORCID 0000-0001-5944-3365
Theodore JardetzkyStanford University School of Medicine, Stanford, CA, USA.
Valerie VerhasseltSchool of Molecular Sciences, University of Western Australia, Perth, WA, Australia.ORCID 0000-0002-5732-9048
Stephen R DurhamImperial College London, National Heart & Lung Institute, London, UK.ORCID 0000-0001-5264-6207
Peter A WürtzenALK, Hørsholm, Denmark.
R J Joost van NeervenWageningen University & Research, Wageningen, The Netherlands.ORCID 0000-0002-3991-5297
Imperial College London · GBALK-Abelló (Denmark) · DKFrieslandCampina (Netherlands) · NLSechenov University · RUStanford University · USThe University of Western Australia · AU

Funding

Accelerated dissociation of IgE receptor complexesR01AI115469 · NIAID · STANFORD UNIVERSITY · PI Theodore S Jardetzky · 2017 to 2026
$3.8M
Suppression of basophil activation by IgE glycovariantsR01HL141493 · NHLBI · STANFORD UNIVERSITY · PI JARDETZKY, THEODORE S · 2018 to 2021
$1.6M
Medical Research Council G0601303NHLBI NIH HHS R01 HL141493NIAID NIH HHS R01 AI115469
6 · The paper itself

Abstract

Immunoglobulin E (IgE)-mediated allergy is the most common hypersensitivity disease affecting more than 30% of the population. Exposure to even minute quantities of allergens can lead to the production of IgE antibodies in atopic individuals. This is termed allergic sensitization, which occurs mainly in early childhood. Allergen-specific IgE then binds to the high (FcεRI) and low-affinity receptors (FcεRII, also called CD23) for IgE on effector cells and antigen-presenting cells. Subsequent and repeated allergen exposure increases allergen-specific IgE levels and, by receptor cross-linking, triggers immediate release of inflammatory mediators from mast cells and basophils whereas IgE-facilitated allergen presentation perpetuates T cell-mediated allergic inflammation. Due to engagement of receptors which are highly selective for IgE, even tiny amounts of allergens can induce massive inflammation. Naturally occurring allergen-specific IgG and IgA antibodies usually recognize different epitopes on allergens compared with IgE and do not efficiently interfere with allergen-induced inflammation. However, IgG and IgA antibodies to these important IgE epitopes can be induced by allergen-specific immunotherapy or by passive immunization. These will lead to competition with IgE for binding with the allergen and prevent allergic responses. Similarly, anti-IgE treatment does the same by preventing IgE from binding to its receptor on mast cells and basophils. Here, we review the complex interplay of allergen-specific IgE, IgG and IgA and the corresponding cell receptors in allergic diseases and its relevance for diagnosis, treatment and prevention of allergy.

Indexed as

Hypersensitivity, ImmediateImmunoglobulin EAllergensChild, PreschoolHumansImmunoglobulin AImmunoglobulin GReceptors, IgEAllergensImmunoglobulin AImmunoglobulin EImmunoglobulin GReceptors, IgEallergy treatmentbasic mechanisms in allergybiologicsbiomarkersIgEimmunotherapytolerance inductionvaccines and mechanisms

Identifiers

PMID33999439
PMCPMC8601105
OpenAlexW3160325999

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.