Evidence map›Paper›PMID 22930820›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2012

Antibodies and IL-3 support helminth-induced basophil expansion.

Tina Herbst, Julia Esser, Moira Prati, Manuel Kulagin, Rebecca Stettler, Mario M Zaiss, James P Hewitson, Patrick Merky, Joseph S Verbeek, Carole Bourquin and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

27 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Trickle infection withFrontiers in immunology · 2022
    Article
  5. Basophils as a potential therapeutic target in cancer.Journal of Zhejiang University. Science. B · 2021
    Review
  6. Diverse innate stimuli activate basophils through pathways involving Syk and IκB kinases.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  7. Basophils in antihelminth immunity.Seminars in immunology · 2021
    Review
  8. BHLHE40 Promotes TJournal of immunology (Baltimore, Md. : 1950) · 2020
    Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Negative Regulation of Type 2 Immunity.Trends in immunology · 2017
    Review
  14. Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Basophil-mediated protection against gastrointestinal helminths requires IgE-induced cytokine secretion.Proceedings of the National Academy of Sciences of the United States of America · 2014
    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

15 authors at 6 institutions in 4 countries.

Tina HerbstInstitute of Microbiology, Swiss Federal Institute of Technology, 8093 Zurich, Switzerland.
Julia Esser
Moira Prati
Manuel Kulagin
Rebecca Stettler
Mario M Zaiss
James P Hewitson
Patrick Merky
Joseph S Verbeek
Carole Bourquin
Mali Camberis
Melanie Prout
Rick M Maizels
Graham Le Gros
Nicola L Harris
Swiss Vaccine Research Institute · CHMalaghan Institute of Medical Research · NZÉcole Polytechnique Fédérale de Lausanne · CHUniversity of Edinburgh · GBLeiden University Medical Center · NLUniversity of Fribourg · CH

Funding

Wellcome Trust 095831
6 · The paper itself

Abstract

Basophils are powerful mediators of Th2 immunity and are present in increased numbers during allergic inflammation and helminth infection. Despite their ability to potentiate Th2 immunity the mechanisms regulating basophil development remain largely unknown. We have found a unique role for isotype-switched antibodies in promoting helminth-induced basophil production following infection of mice with Heligmosomoides polygyrus bakeri or Nippostrongylus brasiliensis. H. polygyrus bakeri-induced basophil expansion was found to occur within the bone marrow, and to a lesser extent the spleen, and was IL-3 dependent. IL-3 was largely produced by CD4(+)CD49b(+)NK1.1(-) effector T cells at these sites, and required the IL-4Rα chain. However, antibody-deficient mice exhibited defective basophil mobilization despite intact T-cell IL-3 production, and supplementation of mice with immune serum could promote basophilia independently of required IL-4Rα signaling. Helminth-induced eosinophilia was not affected by the deficiency in isotype-switched antibodies, suggesting a direct effect on basophils rather than through priming of Th2 responses. Although normal type 2 immunity occurred in the basopenic mice following primary infection with H. polygyrus bakeri, parasite rejection following challenge infection was impaired. These data reveal a role for isotype-switched antibodies in promoting basophil expansion and effector function following helminth infection.

Indexed as

AnimalsAntibodies, HelminthBasophilsImmunoglobulin Class SwitchingInterleukin-3MiceMice, Mutant StrainsNematospiroides dubiusNippostrongylusStatistics, NonparametricStrongylida InfectionsTh2 CellsAntibodies, HelminthInterleukin-3

Identifiers

PMID22930820
PMCPMC3443190
OpenAlexW2100869499

What OpenQuestion holds

Textmetadata
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.