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* Lung Disease Research Group, Departments of Medicine and Pharmacology, University of Melbourne, Victoria, Australia; Ludwig Institute for Cancer Research, Melbourne Tumour Biology Branch, Royal Melbourne Hospital, Victoria, Australia; Department of Medicine, Cooperative Research Centre for Chronic Inflammatory Diseases, Royal Melbourne Hospital, Victoria, Australia; Centre for Child Health Research, University of Western Australia, Perth, Australia; and ¶ Walter and Eliza Hall Institute of Medical Research, Royal Melbourne Hospital, Victoria, Australia
The etiology of asthma, a chronic inflammatory disorder of the airways, remains obscure, although T cells appear to be central disease mediators. Lyn tyrosine kinase has been implicated as both a facilitator and inhibitor of signaling pathways that play a role in allergic inflammation, although its role in asthma is unclear because Lyn is not expressed in T cells. We show in the present study that Lyn–/– mice develop a severe, persistent inflammatory asthma-like syndrome with lung eosinophilia, mast cell hyperdegranulation, intensified bronchospasm, hyper IgE, and Th2-polarizing dendritic cells. Dendritic cells from Lyn–/– mice have a more immature phenotype, exhibit defective inhibitory signaling pathways, produce less IL-12, and can transfer disease when adoptively transferred into wild-type recipients. Our results show that Lyn regulates the intensity and duration of multiple asthmatic traits and indicate that Lyn is an important negative regulator of Th2 immune responses.
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