You are not currently logged in.
Access JSTOR through your library or other institution:
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
New Series, Vol. 282, No. 5397 (Dec. 18, 1998), pp. 2258-2261
Published by: American Association for the Advancement of Science
Stable URL: http://www.jstor.org/stable/2897134
Page Count: 4
You can always find the topics here!Topics: Allergies, Asthma, Mice, Ova, Mucus, Antigens, Cytokines, Eosinophils, T lymphocytes, Animal models
Were these topics helpful?See somethings inaccurate? Let us know!
Select the topics that are inaccurate.
Preview not available
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.
Science © 1998 American Association for the Advancement of Science