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Sarah-Jane E Beavitt, Kenneth W Harder, Joanna M Kemp, Jessica Jones, Cathy Quilici, Franca Casagranda, Ellen Lam, Debra Turner, Siobhain Brennan, Peter D Sly, David M Tarlinton, Gary P Anderson, Margaret L Hibbs, Lyn-Deficient Mice Develop Severe, Persistent Asthma: Lyn Is a Critical Negative Regulator of Th2 Immunity, The Journal of Immunology, Volume 175, Issue 3, August 2005, Pages 1867–1875, https://doi.org/10.4049/jimmunol.175.3.1867
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Abstract
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.
