Evidence map›Paper›PMID 42431517›Full record

ArticleThe Journal of allergy and clinical immunology2026

IgE-sensitized mast cells release extracellular vesicles that transfer IgE and spread allergic sensitization.

Annika Pfeiffer, Geethani Bandara, Kelly Pardo, Gwendolyn Cooper, Benjamin Schwarz, Ian S LaCroix, Eric Bohrnsen, Ellen Zektser, Linda Pham, Fernanda D Young and 11 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of allergy and clinical immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. 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

21 authors.

Annika PfeifferLaboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Bethesda, Md. Electronic address: annika.pfeiffer@nih.gov.
Geethani BandaraLaboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Bethesda, Md.
Kelly PardoLaboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Bethesda, Md.
Gwendolyn CooperResearch Technologies Branch, NIAID, NIH, Hamilton, Mont.
Benjamin SchwarzResearch Technologies Branch, NIAID, NIH, Hamilton, Mont.
Ian S LaCroixResearch Technologies Branch, NIAID, NIH, Hamilton, Mont; Axle Informatics Contracting Agency at NIAID.
Eric BohrnsenResearch Technologies Branch, NIAID, NIH, Hamilton, Mont.
Ellen ZektserLaboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Bethesda, Md.
Linda PhamLaboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Bethesda, Md; Guidehouse Contracting Agency at NIAID, Bethesda, Md.
Fernanda D YoungLaboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Bethesda, Md.
Brian A SellersNIH Center for Human Immunology, Autoimmunity, and Inflammation (CHI), NIH, Bethesda, Md.
Elisabeth MeyerIntegrated Data Sciences Section, Research Technologies Branch, NIAID, NIH, Bethesda, Md; Axle Informatics Contracting Agency at NIAID.
Thomas J LangowskiNIH Center for Human Immunology, Autoimmunity, and Inflammation (CHI), NIH, Bethesda, Md; Axle Informatics Contracting Agency at NIAID.
Min Jenny LiLaboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Bethesda, Md.
Lindsay ChatmanLaboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Bethesda, Md; Kelly Contracting Agency at NIAID.
Karen LakyLaboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Bethesda, Md.
Andrea LukerLaboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Bethesda, Md.
Margery G SmelkinsonResearch Technologies Branch, NIAID, NIH, Bethesda, Md.
Dean D MetcalfeLaboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Bethesda, Md.
Pamela A Frischmeyer-GuerrerioLaboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Bethesda, Md.
Ana OliveraLaboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Bethesda, Md.

Funding

Identification and Characterization of Signaling Pathways and Mediators Regulating Mast Cell-Related DisordersZIAAI001206 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI OLIVERA, ANA · 2015 to 2025
$11.3M
Intramural NIH HHS ZIA AI001206
6 · The paper itself

Abstract

backgroundElevated IgE levels are linked to allergic conditions. IgE binding to FcεRI sensitizes mast cells (MCs), and allergen-induced cross-linking of IgE-bound FcεRI triggers MC activation. Extracellular vesicles (EVs), implicated in intercellular communication, are coreleased during IgE-mediated MC degranulation. Although extensive research has examined MC activation, the effects of IgE sensitization alone on MCs remain less understood.

objectiveWe sought to investigate how IgE sensitization of MCs, without inducing degranulation, affects the quantity, molecular composition, and potential functions of released EVs.

methodsEVs from IgE-sensitized cultured MCs or present in human plasma were isolated by differential ultracentrifugation and quantified by nanoparticle tracking. The molecular composition of MC EVs was analyzed by proteomics, lipidomics, and biochemical assays. Naive MCs were incubated with IgE-containing EVs, and IgE transfer from EVs to recipient cells was tested by flow cytometry, immunoblotting, and cell activation.

resultsIgE sensitization altered quantity and composition of MC EVs. EVs derived from IgE-sensitized MCs exhibited distinct molecular signatures compared to EVs from degranulated MCs. Unlike EVs released during degranulation, these EVs displayed surface-exposed IgE capable of binding antigen and transferred functional IgE complexes to previously unsensitized MCs, thereby conferring activation potential.

conclusionIgE sensitization of MCs induces the release of IgE-containing EVs with distinct molecular signatures, demonstrating that IgE binding has functional consequences and revealing a previously unrecognized mechanism for the dissemination of IgE. This study advances our understanding of MC biology and highlights EVs from IgE-sensitized MCs as amplifiers of allergic sensitization, immune cell communication, and potential biomarkers in allergic diseases.

Indexed as

Allergic sensitizationextracellular vesiclesFcεRIimmunoglobulin Emast cell

Identifiers

PMID42431517
PMCPMC13392823

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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.