IL-33 and Airway Inflammation.
- Author:
Keisuke OBOKI
1
;
Susumu NAKAE
;
Kenji MATSUMOTO
;
Hirohisa SAITO
Author Information
- Publication Type:Review
- Keywords: IL-33; ST2; host defense; allergy; autoimmunity; chronic disease; mast cell; basophil; eosinophil
- MeSH: Asthma; Autoimmunity; Basophils; Chemokines; Chronic Disease; Cytokines; Eosinophils; Epithelial Cells; Humans; Hypersensitivity; Immunoglobulin E; Inflammation; Interleukin-1; Interleukin-18; Mast Cells; Neutrophils; Th1 Cells; Th17 Cells
- From:Allergy, Asthma & Immunology Research 2011;3(2):81-88
- CountryRepublic of Korea
- Language:English
- Abstract: Interleukin-33 (IL-33) is the 11th member of IL-1 cytokine family which includes IL-1 and IL-18. Unlike IL-1beta and IL-18, IL-33 is suggested to function as an alarmin that is released upon endothelial or epithelial cell damage and may not enhance acquired immune responses through activation of inflammasome. ST2, a IL-33 receptor component, is preferentially expressed by T-helper type (Th) 2 cells, mast cells, eosinophils and basophils, compared to Th1 cells, Th17 cells and neutrophils. Thus, IL-33 profoundly enhances allergic inflammation through increased expression of proallergic cytokines and chemokines. Indeed, IL-33 and its receptor genes are recognized as the most susceptible genes for asthma by several recent genomewide association studies. It has also recently been shown that IL-33 plays a crucial role in innate eosinophilic airway inflammation rather than acquired immune responses such as IgE production. As such, IL-33 provides a unique therapeutic way for asthma, i.e., ameliorating innate airway inflammation.
