Interleukin-13: Central Mediator of Allergic Asthma-Reference-Cited by-同舟云学术

Interleukin-13: Central Mediator of Allergic Asthma

Published:1998-12-18 Issue:5397 Volume:282 Page:2258-2261
ISSN:0036-8075
Container-title:Science
language:en
Short-container-title:Science

Author:

Wills-Karp Marsha¹,Luyimbazi Jackie¹,Xu Xueying¹,Schofield Brian¹,Neben Tamlyn Y.¹,Karp Christopher L.¹,Donaldson Debra D.¹

Affiliation:

1. M. Wills-Karp, J. Luyimbazi, X. Xu, B. Schofield, Department of Environmental Health Sciences, Johns Hopkins University School of Hygiene and Public Health, Baltimore, MD 21205, USA. T. Y. Neben and D. D. Donaldson, Immunology Department, Genetics Institute, Cambridge, MA 02140, USA. C. L. Karp, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA, and Department of Molecular Microbiology and Immunology, Johns Hopkins University School of Hygiene and Public...

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.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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