ABSTRACT
The last several years have contributed explosively to our understanding of the pathogenesis of experimental asthma. Coincidentally, a previous generation of human and experimental studies has culminated in a series of ambitious asthma clinical trials that aim to interrupt disease by inhibiting key inflammatory pathways. The results of these trials have been less than extraordinary (1-4), suggesting that, at least during established disease, inflammatory molecules such as interleukin 4 (IL-4), immunoglobulin E (IgE), and IL-5 may not be as critical as once believed. The more recent murine studies now propose that distinct inflammatory molecules and rather different pathogenic mechanisms may underlie allergic asthma. What are these new asthma mediators and disease pathways, and are their prospects for therapeutic targeting any brighter than those previously identified? I will first consider new findings that implicate the cytokines IL-4 and IL-13 and their related signaling pathway in experimental asthma. In the final part of this chapter I discuss the prospects of future therapies based on this unique family of molecules.
