| First Author | Mattes J | Year | 2001 |
| Journal | J Immunol | Volume | 167 |
| Issue | 3 | Pages | 1683-92 |
| PubMed ID | 11466392 | Mgi Jnum | J:120464 |
| Mgi Id | MGI:3706616 | Doi | 10.4049/jimmunol.167.3.1683 |
| Citation | Mattes J, et al. (2001) IL-13 induces airways hyperreactivity independently of the IL-4R alpha chain in the allergic lung. J Immunol 167(3):1683-92 |
| abstractText | 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. |
