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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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Arch. Dis. Child. Fetal Neonatal Ed. 92, F68-F73
   Abstract »    Full Text »    PDF »
Th2 Cell-Selective Enhancement of Human IL13 Transcription by IL13-1112C>T, a Polymorphism Associated with Allergic Inflammation.
L. Cameron, R. B. Webster, J. M. Strempel, P. Kiesler, M. Kabesch, H. Ramachandran, L. Yu, D. A. Stern, P. E. Graves, I. C. Lohman, et al. (2006)
J. Immunol. 177, 8633-8642
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Allergy-Driven Alternative Splicing of IL-13 Receptor {alpha}2 Yields Distinct Membrane and Soluble Forms.
Y. Tabata, W. Chen, M. R. Warrier, A. M. Gibson, M. O. Daines, and G. K. K. Hershey (2006)
J. Immunol. 177, 7905-7912
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CD38-deficient mice have reduced airway hyperresponsiveness following IL-13 challenge.
A. G. P. Guedes, J. Paulin, L. Rivero-Nava, H. Kita, F. E. Lund, and M. S. Kannan (2006)
Am J Physiol Lung Cell Mol Physiol 291, L1286-L1293
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Interleukin-17 is a negative regulator of established allergic asthma.
S. Schnyder-Candrian, D. Togbe, I. Couillin, I. Mercier, F. Brombacher, V. Quesniaux, F. Fossiez, B. Ryffel, and B. Schnyder (2006)
J. Exp. Med. 203, 2715-2725
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A3 Adenosine Receptor Signaling Contributes to Airway Mucin Secretion after Allergen Challenge.
H. W. J. Young, C.-X. Sun, C. M. Evans, B. F. Dickey, and M. R. Blackburn (2006)
Am. J. Respir. Cell Mol. Biol. 35, 549-558
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N-linked glycosylation of IL-13R{alpha}2 is essential for optimal IL-13 inhibitory activity.
M. Kioi, S. Seetharam, and R. K. Puri (2006)
FASEB J 20, 2378-2380
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Inhibition of Arginase I Activity by RNA Interference Attenuates IL-13-Induced Airways Hyperresponsiveness.
M. Yang, D. Rangasamy, K. I. Matthaei, A. J. Frew, N. Zimmmermann, S. Mahalingam, D. C. Webb, D. J. Tremethick, P. J. Thompson, S. P. Hogan, et al. (2006)
J. Immunol. 177, 5595-5603
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Novel Approach to Inhibit Asthma-Mediated Lung Inflammation Using Anti-CD147 Intervention.
W. M. Gwinn, J. M. Damsker, R. Falahati, I. Okwumabua, A. Kelly-Welch, A. D. Keegan, C. Vanpouille, J. J. Lee, L. A. Dent, D. Leitenberg, et al. (2006)
J. Immunol. 177, 4870-4879
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Stat5 Expression Is Required for IgE-Mediated Mast Cell Function..
B. O. Barnstein, G. Li, Z. Wang, S. Kennedy, C. Chalfant, H. Nakajima, K. D. Bunting, and J. J. Ryan (2006)
J. Immunol. 177, 3421-3426
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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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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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Effect of a CD4-Depleting Antibody on the Development of Cryptococcus neoformans-Induced Allergic Bronchopulmonary Mycosis in Mice.
S. Arora, R. A. McDonald, G. B. Toews, and G. B. Huffnagle (2006)
Infect. Immun. 74, 4339-4348
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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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Type 2 immunity is controlled by IL-4/IL-13 expression in hematopoietic non-eosinophil cells of the innate immune system.
D. Voehringer, T. A. Reese, X. Huang, K. Shinkai, and R. M. Locksley (2006)
J. Exp. Med. 203, 1435-1446
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Contribution of IL-18-induced innate T cell activation to airway inflammation with mucus hypersecretion and airway hyperresponsiveness.
Y. Ishikawa, T. Yoshimoto, and K. Nakanishi (2006)
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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