TY  - JOUR
AU  - Beavitt, SJE
AU  - Harder, KW
AU  - Kemp, JM
AU  - Jones, J
AU  - Quilici, C
AU  - Casagranda, F
AU  - Lam, E
AU  - Turner, D
AU  - Brennan, S
AU  - Sly, PD
AU  - Tarlinton, DM
AU  - Anderson, GP
AU  - Hibbs, ML
Y2  - 2014/05/21
Y1  - 2005/08/01
SN  - 0022-1767
UR  - http://hdl.handle.net/11343/26123
AB  - 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.
LA  - English
PB  - AMER ASSOC IMMUNOLOGISTS
KW  - Oncology and Carcinogenesis; Cancer and Related Disorders
T1  - Lyn-deficient mice develop severe, persistent asthma: Lyn is a critical negative regulator of Th2 immunity
DO  - 10.4049/jimmunol.175.3.1867
IS  - Journal of Immunology
VL  - 175
IS  - 3
SP  - 1867-1875
L1  - /bitstream/handle/11343/26123/115885_4922.pdf?sequence=1&isAllowed=n
ER  -