Endogenous IL-33 enhances Th2 cytokine production and T-cell responses during allergic airway inflammation
Open Access
- 21 March 2011
- journal article
- research article
- Published by Oxford University Press (OUP) in International Immunology
- Vol. 23 (5), 307-315
- https://doi.org/10.1093/intimm/dxr006
Abstract
IL-33 is an IL-1-related cytokine which has been implicated in Th2-associated biology and allergic diseases in humans and mice. IL-33 stimulates Th2 cells, mast cells, eosinophils, basophils, iNKT cells and circulating CD34+ stem cells to proliferate and produce pro-allergic cytokines such as IL-5 and IL-13. IL-33 mediates its cytokine effects through a receptor consisting of ST2 and IL-1RAcP. Whereas IL-1RAcP is ubiquitously expressed, ST2 expression is cell-type restricted and determines responsiveness to IL-33. Studies employing ST2-deficient mice have reported variable results on the role of this receptor, and consequently IL-33, with regards to allergic lung inflammation. In this study, we demonstrate that IL-33 is important for allergic lung inflammation. Intra-nasal administration of IL-33 triggered an immediate allergic response in the airways, and more importantly, we show that endogenous IL-33 contributes to airway inflammation and peripheral antigen-specific responses in ovalbumin-induced acute allergic lung inflammation using IL-33-deficient mice. Our results suggest that IL-33 is sufficient and required for severe allergic inflammation in the lung and support the concept of IL-33 as a therapeutic target in allergic lung inflammation.Keywords
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