| First Author | Beavitt SJ | Year | 2005 |
| Journal | J Immunol | Volume | 175 |
| Issue | 3 | Pages | 1867-75 |
| PubMed ID | 16034130 | Mgi Jnum | J:107272 |
| Mgi Id | MGI:3620486 | Doi | 10.4049/jimmunol.175.3.1867 |
| Citation | Beavitt SJ, et al. (2005) Lyn-deficient mice develop severe, persistent asthma: Lyn is a critical negative regulator of Th2 immunity. J Immunol 175(3):1867-75 |
| abstractText | 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. |
