IL-2-Agonist-Induced IFN-γ Exacerbates Systemic Anaphylaxis in Food Allergen-Sensitized Mice

Food allergies are common, costly and potentially life-threatening disorders. They are driven by Th2, but inhibited by Th1 reactions. There is also evidence indicating that IL-2 agonist treatment inhibits allergic sensitization through expansion of regulatory T cells. Here, we tested the impact of a...

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Veröffentlicht in:Frontiers in immunology Jg. 11; S. 596772
Hauptverfasser: Link, Christopher W.M., Rau, Christina N., Udoye, Christopher C., Ragab, Mohab, Korkmaz, Rabia Ü., Comdühr, Sara, Clauder, Ann-Katrin, Lindemann, Timo, Frehse, Britta, Hofmann, Katharina, Almeida, Larissa N., Laumonnier, Yves, Beidaq, Asmaa El, Finkelman, Fred D., Manz, Rudolf A.
Format: Journal Article
Sprache:Englisch
Veröffentlicht: Switzerland Frontiers Media S.A 11.12.2020
Schlagworte:
Allergens - immunology
anaphylaxis
Anaphylaxis - etiology
Anaphylaxis - metabolism
Animals
Chickens
Cytokines - metabolism
Disease Models, Animal
Egg White - adverse effects
Female
Food - adverse effects
food allergy
Food Hypersensitivity - immunology
IFN-γ
IL-2
Immunization
Immunoglobulin E - blood
Immunoglobulin E - immunology
Immunology
Interferon-gamma - metabolism
Interleukin-2 - agonists
Mice
murine model
IFN-γ
IL-2
anaphylaxis
murine model
food allergy
ISSN:1664-3224, 1664-3224
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Zusammenfassung:Food allergies are common, costly and potentially life-threatening disorders. They are driven by Th2, but inhibited by Th1 reactions. There is also evidence indicating that IL-2 agonist treatment inhibits allergic sensitization through expansion of regulatory T cells. Here, we tested the impact of an IL-2 agonist in a novel model for food allergy to hen´s egg in mice sensitized without artificial adjuvants. Prophylactic IL-2 agonist treatment expanded Treg populations and inhibited allergen-specific sensitization. However, IL-2 agonist treatment of already sensitized mice increased mast cell responses and allergic anaphylaxis upon allergen re-challenge. These effects depended on allergen-specific IgE and were mediated through IFN-γ, as shown by IgE transfer and blockade of IFN-γ with monoclonal antibodies. These results suggest that although shifting the allergic reaction toward a Treg/Th1 response inhibits allergic sensitization, the prototypic Th1 cytokine IFN-γ promotes mast cell activation and allergen-induced anaphylaxis in individuals that are already IgE-sensitized. Hence, while a Th1 response can prevent the development of food allergy, IFN-γ has the ability to exacerbate already established food allergy.
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These authors have contributed equally to this work and share senior authorship
This article was submitted to Mucosal Immunity, a section of the journal Frontiers in Immunology
These authors have contributed equally to this work and share first authorship
Reviewed by: Hans Oettgen, Boston Children’s Hospital and Harvard Medical School, United States; Franz Puttur, Imperial College London, United Kingdom
Edited by: Eric Cox, Ghent University, Belgium
ISSN:1664-3224
1664-3224
DOI:10.3389/fimmu.2020.596772