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
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.
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 Health,
Baltimore, MD 21205, USA.
*
To whom correspondence should be addressed. E-mail:
mkarp{at}welchlink.welch.jhu.edu
