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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Published in:Frontiers in immunology Vol. 11; p. 596772
Main Authors: 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
Language:English
Published: Switzerland Frontiers Media S.A 11.12.2020
Subjects:
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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Abstract 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.
AbstractList 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.
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.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.
Author Ragab, Mohab
Almeida, Larissa N.
Link, Christopher W.M.
Clauder, Ann-Katrin
Comdühr, Sara
Hofmann, Katharina
Finkelman, Fred D.
Frehse, Britta
Laumonnier, Yves
Beidaq, Asmaa El
Udoye, Christopher C.
Rau, Christina N.
Lindemann, Timo
Manz, Rudolf A.
Korkmaz, Rabia Ü.
AuthorAffiliation 3 Division of Allergy, Immunology and Rheumatology, Department of Internal Medicine, University of Cincinnati College of Medicine and the Division of Immunobiology, Cincinnati Children’s Hospital Medical Center , Cincinnati, OH , United States
1 Institute for Systemic Inflammation Research, University of Lübeck , Lübeck , Germany
2 Institute of Nutritional Medicine, University of Lübeck , Lübeck , Germany
AuthorAffiliation_xml – name: 3 Division of Allergy, Immunology and Rheumatology, Department of Internal Medicine, University of Cincinnati College of Medicine and the Division of Immunobiology, Cincinnati Children’s Hospital Medical Center , Cincinnati, OH , United States
– name: 1 Institute for Systemic Inflammation Research, University of Lübeck , Lübeck , Germany
– name: 2 Institute of Nutritional Medicine, University of Lübeck , Lübeck , Germany
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Keywords IFN-γ
IL-2
anaphylaxis
murine model
food allergy
Language English
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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
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Snippet Food allergies are common, costly and potentially life-threatening disorders. They are driven by Th2, but inhibited by Th1 reactions. There is also evidence...
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StartPage 596772
SubjectTerms 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
Title IL-2-Agonist-Induced IFN-γ Exacerbates Systemic Anaphylaxis in Food Allergen-Sensitized Mice
URI https://www.ncbi.nlm.nih.gov/pubmed/33362780
https://www.proquest.com/docview/2473406008
https://pubmed.ncbi.nlm.nih.gov/PMC7759672
https://doaj.org/article/7fc169ea44d94d96a1607803dd4fa43e
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