Interleukin-13: Central mediator of allergic asthma

Marsha Wills-Karp, Jackie Luyimbazi, Xueying Xu, Brian Schofield, Tamlyn Y. Neben, Christopher L. Karp, Debra D. Donaldson

Research output: Contribution to journalArticle

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.

Original languageEnglish (US)
Pages (from-to)2258-2261
Number of pages4
JournalScience
Volume282
Issue number5397
DOIs
StatePublished - Dec 18 1998

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    Wills-Karp, M., Luyimbazi, J., Xu, X., Schofield, B., Neben, T. Y., Karp, C. L., & Donaldson, D. D. (1998). Interleukin-13: Central mediator of allergic asthma. Science, 282(5397), 2258-2261. https://doi.org/10.1126/science.282.5397.2258