Evidence map›Paper›PMID 29678672›Full record

ArticleEBioMedicine2018

Genetic restriction of antigen-presentation dictates allergic sensitization and disease in humanized mice.

Alina Neunkirchner, Bernhard Kratzer, Cordula Köhler, Ursula Smole, Lukas F Mager, Klaus G Schmetterer, Doris Trapin, Victoria Leb-Reichl, Edward Rosloniec, Ronald Naumann and 5 more

Open access · goldAbstract read
In one paragraph

Article in EBioMedicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.5field-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

20 citing papers in PubMed, 29 citations in OpenAlex.

  1. Trial
  2. Genetic mechanisms of pollinosis: interactions between genes and environmental factors.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
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  15. Similar Allergenicity to DifferentMedicina (Kaunas, Lithuania) · 2019
    Article
  16. The making and function of CAR cells.Immunology letters · 2019
    Review
  17. Article
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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 5 institutions in 3 countries.

Alina NeunkirchnerChristian Doppler Laboratory for Immunomodulation, 1090 Vienna, Austria; Institute of Immunology, Medical University of Vienna, 1090 Vienna, Austria.
Bernhard KratzerChristian Doppler Laboratory for Immunomodulation, 1090 Vienna, Austria; Institute of Immunology, Medical University of Vienna, 1090 Vienna, Austria.
Cordula KöhlerChristian Doppler Laboratory for Immunomodulation, 1090 Vienna, Austria; Institute of Immunology, Medical University of Vienna, 1090 Vienna, Austria.
Ursula SmoleInstitute of Immunology, Medical University of Vienna, 1090 Vienna, Austria.
Lukas F MagerInstitute of Immunology, Medical University of Vienna, 1090 Vienna, Austria.
Klaus G SchmettererInstitute of Immunology, Medical University of Vienna, 1090 Vienna, Austria; Department of Laboratory Medicine, Medical University of Vienna, 1090 Vienna, Austria.
Doris TrapinInstitute of Immunology, Medical University of Vienna, 1090 Vienna, Austria.
Victoria Leb-ReichlInstitute of Immunology, Medical University of Vienna, 1090 Vienna, Austria.
Edward RosloniecDepartment of Medicine, University of Tennessee Health Science Center, Memphis, 38163, TN, USA; Memphis Veterans Affairs Medical Center, 38104, TN, USA; Department of Pathology, University of Tennessee Health Science Center, Memphis, 38163, TN, USA.
Ronald NaumannMax Planck Institute for Molecular Cell Biology and Genetics, 01307 Dresden, Germany.
Lukas KennerDepartment of Laboratory Animal Pathology, Medical University of Vienna, 1090 Vienna, Austria; Department of Laboratory Animal Pathology, University of Veterinary Medicine Vienna, 1210 Vienna, Austria; Ludwig Boltzmann Institute for Cancer Research, Vienna, Austria.
Beatrice Jahn-SchmidDepartment of Pathophysiology and Allergy Research, Medical University of Vienna, 1090 Vienna, Austria.
Barbara BohleChristian Doppler Laboratory for Immunomodulation, 1090 Vienna, Austria; Department of Pathophysiology and Allergy Research, Medical University of Vienna, 1090 Vienna, Austria.
Rudolf ValentaDepartment of Pathophysiology and Allergy Research, Medical University of Vienna, 1090 Vienna, Austria.
Winfried F PicklChristian Doppler Laboratory for Immunomodulation, 1090 Vienna, Austria; Institute of Immunology, Medical University of Vienna, 1090 Vienna, Austria. Electronic address: winfried.pickl@meduniwien.ac.at.
Medical University of Vienna · ATChristian Doppler Laboratory for Thermoelectricity · ATMax Planck Institute of Molecular Cell Biology and Genetics · DEUniversity of Tennessee Health Science Center · USUniversity of Veterinary Medicine Vienna · AT

Funding

Austrian Science Fund FWF F 1807-B13Austrian Science Fund FWF F 4605Austrian Science Fund FWF F 4609Austrian Science Fund FWF F 4610Austrian Science Fund FWF W 1248
6 · The paper itself

Abstract

backgroundImmunoglobulin(Ig)E-associated allergies result from misguided immune responses against innocuous antigens. CD4

objectiveTo determine the key factors for sensitization and allergy towards a given allergen.

methodsWe here created a novel human T cell receptor(TCR) and human leucocyte antigen (HLA)-DR1 (TCR-DR1) transgenic mouse model of asthma, based on the human-relevant major mugwort (Artemisia vulgaris) pollen allergen Art v 1 to examine the critical factors for sensitization and allergy upon natural allergen exposure via the airways in the absence of systemic priming and adjuvants.

resultsAcute allergen exposure led to IgE-independent airway hyperreactivity (AHR) and T helper(Th)2-prone lung inflammation in TCR-DR1, but not DR1, TCR or wildtype (WT) control mice, that was alleviated by prophylactic interleukin(IL)-2-αIL-2 mAb complex-induced expansion of Tregs. Chronic allergen exposure sensitized one third of single DR1 transgenic mice, however, without impacting on lung function. Similar treatment led to AHR and Th2-driven lung pathology in >90% of TCR-DR1 mice. Prophylactic and therapeutic expansion of Tregs with IL-2-αIL-2 mAb complexes blocked the generation and boosting of allergen-specific IgE associated with chronic allergen exposure.

conclusionsWe identify genetic restriction of allergen presentation as primary factor dictating allergic sensitization and disease against the major pollen allergen from the weed mugwort, which frequently causes sensitization and disease in humans. Furthermore, we demonstrate the importance of the balance between allergen-specific T effector and Treg cells for modulating allergic immune responses.

Indexed as

HypersensitivityImmunoglobulin EReceptors, AntigenTh2 CellsAnimalsAntigen PresentationAntigens, PlantHumansMiceMice, TransgenicPlant ProteinsAntigens, PlantArt v 1 protein, mugwortImmunoglobulin EPlant ProteinsReceptors, AntigenAeroallergenAirway hyperreactivityAllergen-specific TCRIL-2-αIL-2 complexesMugwort allergySensitizationToleranceT regulatory cells

Identifiers

PMID29678672
PMCPMC6014064
OpenAlexW2795839893

What OpenQuestion holds

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LicenceCC BY
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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.