Abstract
In complex disorders such as asthma and allergic disease, the goal for developing disease-modifying biotherapeutics is to find a target that is a central instigator of immunologic activity. Interleukin (IL)-33 seems to be such a molecule, as it is one of the earliest-released signaling molecules following epithelial damage and can orchestrate the recruitment and activation of the cells responsible for disease. Unregulated IL-33 activity leads to activation of T-helper type 2 cells, mast cells, dendritic cells, eosinophils, and basophils, ultimately leading to increased expression of cytokines and chemokines that define the disease. As such, IL-33 is an attractive candidate for therapeutic intervention with the goal of ameliorating disease. This review focuses on the role of IL-33 in promoting and maintaining the asthma phenotype.
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Acknowledgment
Dr. Steinke has received grant support from the National Institutes of Health.
Disclosure
Dr. Borish has served as a consultant for Regeneron Pharmaceuticals, Cephalon, and Hoffmann-LaRoche; has received grant support from Genentech and Merck & Co.; has received honoraria from Merck & Co.; and has had travel/accommodation expenses covered by Merck & Co.
Dr. Steinke has served as a consultant for CAT Consulting and has received payment for development of educational presentations from the American Academy of Allergy, Asthma, and Immunology; the American College of Allergy, Asthma, and Immunology; and the World Allergy Organization.
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Borish, L., Steinke, J.W. Interleukin-33 in Asthma: How Big of a Role Does It Play?. Curr Allergy Asthma Rep 11, 7–11 (2011). https://doi.org/10.1007/s11882-010-0153-8
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DOI: https://doi.org/10.1007/s11882-010-0153-8