Evidence map›Paper›PMID 34996839›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2022

Siglec-F Promotes IL-33-Induced Cytokine Release from Bone Marrow-Derived Eosinophils Independently of the ITIM and ITIM-like Motif Phosphorylation.

Stefanie Westermann, Axel Dietschmann, Daniela Doehler, Kirstin Castiglione, Bruce S Bochner, David Voehringer, Daniel Radtke

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.1field-weighted citation impact, top 25% 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

11 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Article
  3. Mucins and Their Roles in Asthma.Immunological reviews · 2025
    Review
  4. IL-33-Induced TREM2Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Siglecs in allergy and asthma.Molecular aspects of medicine · 2023
    Review
  11. Review
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 2 institutions in 2 countries.

Stefanie WestermannDepartment of Infection Biology, University Hospital Erlangen and Friedrich-Alexander University Erlangen-Nuremberg, Erlangen, Germany; and.ORCID 0000-0003-4977-0009
Axel DietschmannDepartment of Infection Biology, University Hospital Erlangen and Friedrich-Alexander University Erlangen-Nuremberg, Erlangen, Germany; and.ORCID 0000-0002-0598-9714
Daniela DoehlerDepartment of Infection Biology, University Hospital Erlangen and Friedrich-Alexander University Erlangen-Nuremberg, Erlangen, Germany; and.
Kirstin CastiglioneDepartment of Infection Biology, University Hospital Erlangen and Friedrich-Alexander University Erlangen-Nuremberg, Erlangen, Germany; and.
Bruce S BochnerDivision of Allergy and Immunology, Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL.ORCID 0000-0002-9411-6009
David VoehringerDepartment of Infection Biology, University Hospital Erlangen and Friedrich-Alexander University Erlangen-Nuremberg, Erlangen, Germany; and david.voehringer@uk-erlangen.de.ORCID 0000-0001-6650-0639
Daniel RadtkeDepartment of Infection Biology, University Hospital Erlangen and Friedrich-Alexander University Erlangen-Nuremberg, Erlangen, Germany; and.ORCID 0000-0003-3241-4542
Friedrich-Alexander-Universität Erlangen-Nürnberg · DENorthwestern University · US

Funding

Using siglecs and their ligands to treat allergic diseases SALTADU19AI136443 · NIAID · NORTHWESTERN UNIVERSITY AT CHICAGO · PI BOCHNER, BRUCE S · 2018 to 2022
$7.6M
NIAID NIH HHS U19 AI136443
6 · The paper itself

Abstract

Eosinophils are potent innate effector cells associated mainly with type 2 immune responses elicited by helminths and allergens. Their activity needs to be tightly controlled to prevent severe inflammation and tissue damage. Eosinophil degranulation and secretion of inflammatory effector molecules, including cytokines, chemokines, and lipid mediators, can be regulated by activating and inhibitory receptors on the cell surface. In this study, we investigated the modulation of proliferation, apoptosis, gene expression, and cytokine/chemokine secretion from IL-33-activated

Indexed as

AnimalsApoptosisAspergillosisAspergillus fumigatusBone Marrow CellsCells, CulturedChemokine CCL3Chemokine CCL4EosinophiliaEosinophilsHumansInterleukin-13Interleukin-33Interleukin-4MiceMice, Inbred C57BLCcl3 protein, mouseCcl4 protein, mouseChemokine CCL3Chemokine CCL4Il33 protein, mouseIl4 protein, mouseInterleukin-13Interleukin-33Interleukin-4Sialic Acid Binding Immunoglobulin-like LectinsSiglecf protein, mouseStat6 protein, mouseSTAT6 Transcription Factor

Identifiers

PMID34996839
PMCPMC8852812
OpenAlexW4205798563

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.