Interleukin-13: Central Mediator of Allergic Asthma

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 the...

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Bibliographic Details
Published in:	Science (American Association for the Advancement of Science) Vol. 282; no. 5397; pp. 2258 - 2261
Main Authors:	Wills-Karp, Marsha, Luyimbazi, Jackie, Xu, Xueying, Schofield, Brian, Neben, Tamlyn Y., Karp, Christopher L., Donaldson, Debra D.
Format:	Journal Article
Language:	English
Published:	Washington, DC American Society for the Advancement of Science 18-12-1998 American Association for the Advancement of Science The American Association for the Advancement of Science
Subjects:	Allergens - immunology Allergic diseases Allergies Allergy Animal models Animals Antigens Asthma Asthma - immunology Asthma - pathology Asthma - physiopathology Biological and medical sciences Bronchial Hyperreactivity Bronchoalveolar Lavage Fluid - cytology Cytokines Eosinophils Goblet Cells - pathology Humans Immunoglobulin E - blood Immunopathology Inhibition Interleukin-13 - antagonists & inhibitors Interleukin-13 - pharmacology Interleukin-13 - physiology Interleukin-13 Receptor alpha1 Subunit Interleukin-4 - physiology Interleukins Lung - immunology Lung - pathology Male Medical research Medical sciences Mice Mice, Inbred A Mucus Ova Ovalbumin - immunology Receptors, Interleukin - physiology Receptors, Interleukin-13 Receptors, Interleukin-4 - antagonists & inhibitors Receptors, Interleukin-4 - physiology Recombinant Fusion Proteins - pharmacology Recombinant Proteins - pharmacology Respiratory and ent allergic diseases T lymphocytes Immunopathology Allergy Animal model Pathophysiology Respiratory disease Pathogenesis Rodentia Blocking Interleukin 13 Asthma Vertebrata Mammalia Mouse Obstructive pulmonary disease
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Summary:	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.
Bibliography:	ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 ObjectType-Article-1 ObjectType-Feature-2
ISSN:	0036-8075 1095-9203
DOI:	10.1126/science.282.5397.2258