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Interleukin-13: Central Mediator of Allergic Asthma

Marsha Wills-Karp, Jackie Luyimbazi, Xueying Xu, Brian Schofield, Tamlyn Y. Neben, Christopher L. Karp and Debra D. Donaldson
Science
New Series, Vol. 282, No. 5397 (Dec. 18, 1998), pp. 2258-2261
Stable URL: http://www.jstor.org/stable/2897134
Page Count: 4
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Interleukin-13: Central Mediator of Allergic Asthma
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Abstract

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.

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