| First Author | Wills-Karp M | Year | 1998 |
| Journal | Science | Volume | 282 |
| Issue | 5397 | Pages | 2258-61 |
| PubMed ID | 9856949 | Mgi Jnum | J:109109 |
| Mgi Id | MGI:3625781 | Doi | 10.1126/science.282.5397.2258 |
| Citation | Wills-Karp M, et al. (1998) Interleukin-13: central mediator of allergic asthma. Science 282(5397):2258-61 |
| abstractText | The worldwide incidence, morbidity, and mortality of allergic asthma are increasing. The pathophysiological features of allergic asthma are thought to result from the aberrant expansion of CD4(+) T cells producing the type 2 cytokines interleukin-4 (IL-4) and IL-5, although a necessary role for these cytokines in allergic asthma has not been demonstrable. The type 2 cytokine IL-13, which shares a receptor component and signaling pathways with IL-4, was found to be necessary and sufficient for the expression of allergic asthma. IL-13 induces the pathophysiological features of asthma in a manner that is independent of immunoglobulin E and eosinophils. Thus, IL-13 is critical to allergen-induced asthma but operates through mechanisms other than those that are classically implicated in allergic responses. |
