Asthma is characterised by airway hyperreactivity (AHR), mucus overproduction and chronic eosinophilic inflammation mediated by Th2 lymphocytes, but no single molecule has been identified that could be pivotal to the mechanism of the disease. In 1 July advanced online Nature Medicine, Douglas Kuperman and colleagues at University of California San Francisco, School of Medicine show that direct effects of interleukin-13 on epithelial cells causes AHR and mucus overproduction in asthma.

Kuperman et al. worked with mice lacking signal transducer and activator of transcription 6 (STAT6 – a critical signaling molecule activated by IL-13 receptor ligation) and observed that these animals were protected from AHR, mucus production and eosinophilia normally induced by IL-13. In addition, reconstruction of STAT6 only in epithelial cells was sufficient for IL-13-induced AHR and mucus production, in the absence of inflammation, fibrosis or other lung pathology.

"Our results suggest that blocking these receptors, or the...

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