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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

IL-13 induces airways hyperreactivity independently of the IL-4R alpha chain in the allergic lung.

The potent spasmogenic properties of IL-13 have identified this molecule as a potential regulator of airways hyperreactivity (AHR) in asthma. Although IL-13 is thought to primarily signal through the IL-13Ralpha1-IL-4Ralpha complex, the cellular and molecular components employed by this cytokine to induce AHR in the allergic lung have not been identified. By transferring OVA-specific CD4(+) T cells that were wild type (IL-13(+/+) T cells) or deficient in IL-13 (IL-13(-/-) T cells) to nonsensitized mice that were then challenged with OVA aerosol, we show that T cell-derived IL-13 plays a key role in regulating AHR, mucus hypersecretion, eotaxin production, and eosinophilia in the allergic lung. Moreover, IL-13(+/+) T cells induce these features (except mucus production) of allergic disease independently of the IL-4Ralpha chain. By contrast, IL-13(+/+) T cells did not induce disease in STAT6-deficient mice. This shows that IL-13 employs a novel component of the IL-13 receptor signaling system that involves STAT6, independently of the IL-4Ralpha chain, to modulate pathogenesis. We show that this novel pathway for IL-13 signaling is dependent on T cell activation in the lung and is critically linked to downstream effector pathways regulated by eotaxin and STAT6.[1]


  1. IL-13 induces airways hyperreactivity independently of the IL-4R alpha chain in the allergic lung. Mattes, J., Yang, M., Siqueira, A., Clark, K., MacKenzie, J., McKenzie, A.N., Webb, D.C., Matthaei, K.I., Foster, P.S. J. Immunol. (2001) [Pubmed]
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