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Science 18 December 1998:
Vol. 282. no. 5397, pp. 2258 - 2261
DOI: 10.1126/science.282.5397.2258
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Reports

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

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J. Immunol. 177, 4870-4879
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Opposing Actions of Stat1 and Stat6 on IL-13-Induced Up-Regulation of Early Growth Response-1 and Platelet-Derived Growth Factor Ligands in Pulmonary Fibroblasts.
J. L. Ingram, A. Antao-Menezes, J. B. Mangum, O. Lyght, P. J. Lee, J. A. Elias, and J. C. Bonner (2006)
J. Immunol. 177, 4141-4148
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Persistent Effects Induced by IL-13 in the Lung.
P. C. Fulkerson, C. A. Fischetti, L. M. Hassman, N. M. Nikolaidis, and M. E. Rothenberg (2006)
Am. J. Respir. Cell Mol. Biol. 35, 337-346
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The high-affinity IgE receptor (Fc{epsilon}RI): a critical regulator of airway smooth muscle cells?.
A. S. Gounni (2006)
Am J Physiol Lung Cell Mol Physiol 291, L312-L321
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Role of Local Pulmonary IFN-{gamma} Expression in Murine Allergic Airway Inflammation.
M. Koch, M. Witzenrath, C. Reuter, M. Herma, H. Schutte, N. Suttorp, H. Collins, and S. H. E. Kaufmann (2006)
Am. J. Respir. Cell Mol. Biol. 35, 211-219
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Role of 5-Lipoxygenase in IL-13-Induced Pulmonary Inflammation and Remodeling.
Y. M. Shim, Z. Zhu, T. Zheng, C. G. Lee, R. J. Homer, B. Ma, and J. A. Elias (2006)
J. Immunol. 177, 1918-1924
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Transcription Factors T-bet and GATA-3 Regulate Development of Airway Remodeling.
T. Kiwamoto, Y. Ishii, Y. Morishima, K. Yoh, A. Maeda, K. Ishizaki, T. Iizuka, A. E. Hegab, Y. Matsuno, S. Homma, et al. (2006)
Am. J. Respir. Crit. Care Med. 174, 142-151
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Cytokines or their antagonists for the treatment of asthma..
P. M. O'Byrne (2006)
Chest 130, 244-250
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Immunogenetic Programs for Viral Induction of Mucous Cell Metaplasia.
M. J. Holtzman, J. T. Battaile, and A. C. Patel (2006)
Am. J. Respir. Cell Mol. Biol. 35, 29-39
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Level of Expression of IL-13R{alpha}2 Impacts Receptor Distribution and IL-13 Signaling..
M. O. Daines, Y. Tabata, B. A. Walker, W. Chen, M. R. Warrier, S. Basu, and G. K. K. Hershey (2006)
J. Immunol. 176, 7495-7501
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Contribution of IL-18 to atopic-dermatitis-like skin inflammation induced by Staphylococcus aureus product in mice.
M. Terada, H. Tsutsui, Y. Imai, K. Yasuda, H. Mizutani, K. Yamanishi, M. Kubo, K. Matsui, H. Sano, and K. Nakanishi (2006)
PNAS 103, 8816-8821
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Regulation of Mucin Genes in Chronic Inflammatory Airway Diseases.
J. A. Voynow, S. J. Gendler, and M. C. Rose (2006)
Am. J. Respir. Cell Mol. Biol. 34, 661-665
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