Allergy and ferroptosis

Haiyan Guo; Mingsheng Lei; Jinan Ma; Hongchun Du; Youming Zhang; Haiyan Guo; Mingsheng Lei; Jinan Ma; Hongchun Du; Youming Zhang

doi:10.3934/Allergy.2025002

AIMS Allergy and Immunology

2025, Volume 9, Issue 1: 8-26. doi: 10.3934/Allergy.2025002

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Review

Allergy and ferroptosis

1.
Department of Geriatrics, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, Guangdong, China
2.
Shenzhen Key Laboratory of Systems Medicine for Inflammatory Diseases, Shenzhen, China
3.
Department of Pulmonary and Critical Care Medicine, Zhangjiajie Hospital Affiliated to Hunan Normal University, Zhangjiajie, Hunan, China
4.
Zhangjiajie College, Zhangjiajie, Hunan, China
5.
Department of Oncology, The Second Xiangya Hospital of Central South University, Changsha, China
6.
Department of Pulmonary and Critical Care Medicine, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China
7.
National Heart and Lung Institute, Imperial College London, Dovehouse Street, London SW3 6LY, UK

Received: 26 October 2024 Revised: 15 February 2025 Accepted: 25 February 2025 Published: 06 March 2025

Allergic responses are defined by hypersensitive reactions against foreign antigens that activate immune cell interactions, leading B lymphocytes to produce IgE. This results in tissue mast cells and circulating basophil cells releasing leukotrienes and histamine, which causes an early inflammatory response; in the late phase, immune cells release chemokines and cytokines. Ferroptosis is an iron-dependently regulated cell death process in which excessive production of reactive oxygen species (ROS) causes massive lipid peroxidation–mediated membrane damage. Allergens, IgE regulation, inflammatory cytokines, and lipid metabolism from an allergic response can induce ferroptosis, which can then enhance the allergic response. This review summarizes the mechanism of ferroptosis and its key regulators. We particularly focus on the potential roles of allergen triggers, IgE regulation, inflammatory cytokines, and lipid metabolism in ferroptosis. We also describe recent research progress regarding ferroptosis in allergic asthma, allergic rhinitis, and allergic dermatitis. Further research on the process of ferroptosis in allergic responses and diseases can aid potential novel therapeutic tools.
- allergic response,
- ferroptosis,
- oxidation,
- IgE,
- lipid metabolism
Citation: Haiyan Guo, Mingsheng Lei, Jinan Ma, Hongchun Du, Youming Zhang. Allergy and ferroptosis[J]. AIMS Allergy and Immunology, 2025, 9(1): 8-26. doi: 10.3934/Allergy.2025002

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Abstract

Allergic responses are defined by hypersensitive reactions against foreign antigens that activate immune cell interactions, leading B lymphocytes to produce IgE. This results in tissue mast cells and circulating basophil cells releasing leukotrienes and histamine, which causes an early inflammatory response; in the late phase, immune cells release chemokines and cytokines. Ferroptosis is an iron-dependently regulated cell death process in which excessive production of reactive oxygen species (ROS) causes massive lipid peroxidation–mediated membrane damage. Allergens, IgE regulation, inflammatory cytokines, and lipid metabolism from an allergic response can induce ferroptosis, which can then enhance the allergic response. This review summarizes the mechanism of ferroptosis and its key regulators. We particularly focus on the potential roles of allergen triggers, IgE regulation, inflammatory cytokines, and lipid metabolism in ferroptosis. We also describe recent research progress regarding ferroptosis in allergic asthma, allergic rhinitis, and allergic dermatitis. Further research on the process of ferroptosis in allergic responses and diseases can aid potential novel therapeutic tools.

Acknowledgments

Haiyan Guo was supported by a grant from Guangdong Province for Young Scientist Award for Applied and Basic Research (2019A1515110563). Hongchun Du was supported by a grant from Medical Scientific Research Foundation of Guangdong Province of China (A2024328).

Conflict of interest

The authors declare no conflict of interest.

Author contributions

All authors contributed to write the manuscript. Y.Z finalized the draft.

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