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.
Nematode parasites cause significant infections in both humans and animals. They are complex, multicellular organisms that present unique challenges for the host, in particular with respect to the recognition of their unusual surface structures by the innate defence system. The innate immune system is now recognized to be a critical component in the development of an adaptive effector response as well as a driver of vaccine-induced immunity. This paper will give an overview of current research on the innate barriers and immune mechanisms, cells, and receptors involved in the innate host response to nematode parasites. It will also review the 'nematode-associated molecular patterns' that may be specifically recognized by the host, in addition to other signals, such as nervous stimulation and tissue damage, that may alert the innate system to parasite invasion.
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