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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 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
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
Read the Full Text
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J. Immunol.
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- Murine Cytomegalovirus Influences Foxj1 Expression, Ciliogenesis, and Mucus Plugging in Mice with Allergic Airway Disease.
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Am. J. Pathol.
172, 714-724
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J. Exp. Med.
205, 361-372
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J. Immunol.
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- Gene Expression in Asthmatic Airway Smooth Muscle.
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Proceedings of the ATS
5, 113-118
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- IL-13 Receptor {alpha}2 Selectively Inhibits IL-13-Induced Responses in the Murine Lung.
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Int. Immunol.
18, 847-855
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- Niflumic Acid Suppresses Interleukin-13-induced Asthma Phenotypes.
- T. Nakano, H. Inoue, S. Fukuyama, K. Matsumoto, M. Matsumura, M. Tsuda, T. Matsumoto, H. Aizawa, and Y. Nakanishi (2006)
Am. J. Respir. Crit. Care Med.
173, 1216-1221
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- Factor B of the alternative complement pathway regulates development of airway hyperresponsiveness and inflammation.
- C. Taube, J. M. Thurman, K. Takeda, A. Joetham, N. Miyahara, M. C. Carroll, A. Dakhama, P. C. Giclas, V. M. Holers, and E. W. Gelfand (2006)
PNAS
103, 8084-8089
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- IL-4 Induces In Vivo Production of IFN-{gamma} by NK and NKT Cells.
- S. C. Morris, T. Orekhova, M. J. Meadows, S. M. Heidorn, J. Yang, and F. D. Finkelman (2006)
J. Immunol.
176, 5299-5305
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- Role of CCR5 in the Pathogenesis of IL-13-Induced Inflammation and Remodeling..
- B. Ma, W. Liu, R. J. Homer, P. J. Lee, A. J. Coyle, J. M. Lora, C. G. Lee, and J. A. Elias (2006)
J. Immunol.
176, 4968-4978
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- 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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