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Science 18 December 1998:
Vol. 282. no. 5397, pp. 2261 - 2263
DOI: 10.1126/science.282.5397.2261
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Reports

Requirement for IL-13 Independently of IL-4 in Experimental Asthma

Gabriele Grünig, Martha Warnock, Adil E. Wakil, Rajeev Venkayya, Frank Brombacher, Donna M. Rennick, Dean Sheppard, Markus Mohrs, Debra D. Donaldson, Richard M. Locksley, David B. Corry *

The pathogenesis of asthma reflects, in part, the activity of T cell cytokines. Murine models support participation of interleukin-4 (IL-4) and the IL-4 receptor in asthma. Selective neutralization of IL-13, a cytokine related to IL-4 that also binds to the alpha chain of the IL-4 receptor, ameliorated the asthma phenotype, including airway hyperresponsiveness, eosinophil recruitment, and mucus overproduction. Administration of either IL-13 or IL-4 conferred an asthma-like phenotype to nonimmunized T cell-deficient mice by an IL-4 receptor alpha  chain-dependent pathway. This pathway may underlie the genetic associations of asthma with both the human 5q31 locus and the IL-4 receptor.

G. Grünig, R. Venkayya, D. Sheppard, D. B. Corry, Departments of Medicine and the Lung Biology Center at the San Francisco General Hospital, University of California San Francisco, San Francisco, CA 94143, USA. M. Warnock, Department of Pathology, University of California San Francisco, San Francisco, CA 94143, USA. A. E. Wakil, Department of Transplantation, California Pacific Medical Center, San Francisco, CA 94115, USA. F. Brombacher, Department of Immunology at the Groote Schuur Hospital, University of Cape Town, Cape Town, South Africa. D. M. Rennick, DNAX Research Institute of Molecular and Cellular Biology, Palo Alto, CA 94304, USA. M. Mohrs, Department of Microbiology/Immunology and the Howard Hughes Medical Institute, University of California San Francisco, San Francisco, CA 94143, USA. D. D. Donaldson, Genetics Institute, Cambridge, MA 02140, USA. R. M. Locksley, Departments of Medicine and Microbiology/Immunology, and the Howard Hughes Medical Institute, University of California San Francisco, San Francisco, CA 94143, USA.
*   To whom correspondence should be addressed. E-mail: habari{at}itsa.ucsf.edu

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   Abstract »    Full Text »    PDF »
A Protective Role for the Fifth Complement Component (C5) in Allergic Airway Disease.
S. M. Drouin, M. Sinha, G. Sfyroera, J. D. Lambris, and R. A. Wetsel (2006)
Am. J. Respir. Crit. Care Med. 173, 852-857
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Role of macrophage migration inhibitory factor in ovalbumin-induced airway inflammation in rats.
M. Kobayashi, Y. Nasuhara, A. Kamachi, Y. Tanino, T. Betsuyaku, E. Yamaguchi, J. Nishihira, and M. Nishimura (2006)
Eur. Respir. J. 27, 726-734
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Reversal of Allergen-induced Airway Remodeling by CysLT1 Receptor Blockade.
W. R. Henderson Jr., G. K. S. Chiang, Y.-t. Tien, and E. Y. Chi (2006)
Am. J. Respir. Crit. Care Med. 173, 718-728
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De novo synthesis of early growth response factor-1 is required for the full responsiveness of mast cells to produce TNF and IL-13 by IgE and antigen stimulation.
B. Li, M. R. Power, and T.-J. Lin (2006)
Blood 107, 2814-2820
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Role of Early Growth Response-1 (Egr-1) in Interleukin-13-induced Inflammation and Remodeling.
S. J. Cho, M. J. Kang, R. J. Homer, H. R. Kang, X. Zhang, P. J. Lee, J. A. Elias, and C. G. Lee (2006)
J. Biol. Chem. 281, 8161-8168
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CD4+ invariant T-cell-receptor+ natural killer T cells in bronchial asthma..
O. Akbari, J. L. Faul, E. G. Hoyte, G. J. Berry, J. Wahlstrom, M. Kronenberg, R. H. DeKruyff, and D. T. Umetsu (2006)
N. Engl. J. Med. 354, 1117-1129
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The Leukotriene B4 Receptor (BLT1) Is Required for Effector CD8+ T Cell-Mediated, Mast Cell-Dependent Airway Hyperresponsiveness..
C. Taube, N. Miyahara, V. Ott, B. Swanson, K. Takeda, J. Loader, L. D. Shultz, A. M. Tager, A. D. Luster, A. Dakhama, et al. (2006)
J. Immunol. 176, 3157-3164
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Glycolipid activation of invariant T cell receptor+ NK T cells is sufficient to induce airway hyperreactivity independent of conventional CD4+ T cells.
E. H. Meyer, S. Goya, O. Akbari, G. J. Berry, P. B. Savage, M. Kronenberg, T. Nakayama, R. H. DeKruyff, and D. T. Umetsu (2006)
PNAS 103, 2782-2787
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Splenic Dendritic Cells Induced by Oral Antigen Administration Are Important for the Transfer of Oral Tolerance in an Experimental Model of Asthma.
K. Nagatani, M. Dohi, Y. To, R. Tanaka, K. Okunishi, K. Nakagome, K. Sagawa, Y. Tanno, Y. Komagata, and K. Yamamoto (2006)
J. Immunol. 176, 1481-1489
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