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Soluble ST2 blocks interleukin-33 signaling in allergic airway inflammation.

Authors: Hayakawa, H  Hayakawa, M  Kume, A  Tominaga, S 
Citation: Hayakawa H, etal., J Biol Chem. 2007 Sep 7;282(36):26369-80. Epub 2007 Jul 10.
Pubmed: (View Article at PubMed) PMID:17623648
DOI: Full-text: DOI:10.1074/jbc.M704916200

The ST2 gene produces a soluble secreted form and a transmembrane form, referred to as soluble ST2 and ST2L, respectively. A recent study has reported that interleukin (IL)-33 is a specific ligand of ST2L and induces production of T helper type 2 (Th2) cytokines. Although soluble ST2 is highly produced in sera of asthmatic patients and plays a critical role for production of Th2 cytokines, the function of soluble ST2 in relation to IL-33 signaling remains unclear. Here we show antagonistic effects of soluble ST2 on IL-33 signaling using a murine thymoma EL-4 cells stably expressing ST2L and a murine model of asthma. Soluble ST2 directly bound to IL-33 and suppressed activation of NF-kappaB in EL-4 cells stably expressing ST2L, suggesting that the complex of soluble ST2 and IL-33 fails to bind to ST2L. In a murine model of asthma, pretreatment with soluble ST2 reduced production of IL-4, IL-5, and IL-13 from IL-33-stimulated splenocytes. These results indicate that soluble ST2 acts as a negative regulator of Th2 cytokine production by the IL-33 signaling. Our study provides a molecular mechanism wherein soluble ST2 modulates the biological activity of IL-33 in allergic airway inflammation.


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CRRD Object Information
CRRD ID: 5144235
Created: 2011-08-02
Species: All species
Last Modified: 2011-08-02
Status: ACTIVE


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