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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
Read the Full Text
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- The Immunopathogenesis of Chronic Obstructive Pulmonary Disease: Insights from Recent Research.
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- Allergic Airway Responses in Obese Mice.
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Am. J. Respir. Crit. Care Med.
176, 650-658
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- Neonatal Chlamydial Infection Induces Mixed T-Cell Responses That Drive Allergic Airway Disease.
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Am. J. Respir. Crit. Care Med.
176, 556-564
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- T helper 1 cells stimulated with ovalbumin and IL-18 induce airway hyperresponsiveness and lung fibrosis by IFN-{gamma} and IL-13 production.
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PNAS
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- Central Role of Muc5ac Expression in Mucous Metaplasia and Its Regulation by Conserved 5' Elements.
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Am. J. Respir. Cell Mol. Biol.
37, 273-290
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- Novel Recombinant Interleukin-13 Peptide-based Vaccine Reduces Airway Allergic Inflammatory Responses in Mice.
- Y. Ma, K. T. HayGlass, A. B. Becker, Y. Fan, X. Yang, S. Basu, G. Srinivasan, F. E. R. Simons, A. J. Halayko, and Z. Peng (2007)
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176, 439-445
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- Inhibition of Experimental Allergic Airways Disease by Local Application of a Cell-Penetrating Dominant-Negative STAT-6 Peptide.
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J. Immunol.
179, 2556-2564
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- Resistin-like molecule-beta is an allergen-induced cytokine with inflammatory and remodeling activity in the murine lung.
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Am J Physiol Lung Cell Mol Physiol
293, L305-L313
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- Measurement of IL-13-Induced iNOS-Derived Gas Phase Nitric Oxide in Human Bronchial Epithelial Cells.
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Am. J. Respir. Cell Mol. Biol.
37, 97-104
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- Galectin-9 Inhibits CD44-Hyaluronan Interaction and Suppresses a Murine Model of Allergic Asthma.
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- T-cell co-stimulatory molecules: their role in allergic immune reactions.
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- 4-1BB triggers IL-13 production from T cells to limit the polarized, Th1-mediated inflammation.
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- Lack of lymphoid chemokines CCL19 and CCL21 enhances allergic airway inflammation in mice.
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Int. Immunol.
19, 775-784
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- Comparison of Airway Remodeling in Acute, Subacute, and Chronic Models of Allergic Airways Disease.
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- Remodeling and Airway Hyperresponsiveness but Not Cellular Inflammation Persist after Allergen Challenge in Asthma.
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175, 896-904
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- A deficient TLR2 signaling promotes airway mucin production in Mycoplasma pneumoniae-infected allergic mice.
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Am J Physiol Lung Cell Mol Physiol
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- Airway Exposure Levels of Lipopolysaccharide Determine Type 1 versus Type 2 Experimental Asthma.
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J. Immunol.
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- Lysophosphatidic Acid Induces Interleukin-13 (IL-13) Receptor {alpha}2 Expression and Inhibits IL-13 Signaling in Primary Human Bronchial Epithelial Cells.
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- Superantigen Presentation by Airway Smooth Muscle to CD4+ T Lymphocytes Elicits Reciprocal Proasthmatic Changes in Airway Function.
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- Posttranscriptional Inhibition of Interferon-Gamma Production by Lead.
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- Efficacy of IL-13 Neutralization in a Sheep Model of Experimental Asthma.
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- IL-2 and IL-18 Attenuation of Airway Hyperresponsiveness Requires STAT4, IFN-{gamma}, and Natural Killer Cells.
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Am. J. Respir. Cell Mol. Biol.
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- IL-13 Mediates In Vivo IL-9 Activities on Lung Epithelial Cells but Not on Hematopoietic Cells.
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- Functional Dissection Identifies a Conserved Noncoding Sequence-1 Core That Mediates IL13 and IL4 Transcriptional Enhancement.
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- IL-13 and Epidermal Growth Factor Receptor Have Critical but Distinct Roles in Epithelial Cell Mucin Production.
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Am. J. Respir. Cell Mol. Biol.
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