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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

Allergic asthma is a complex disorder characterized by local and systemic allergic inflammation and reversible airway obstruction. Asthma symptoms, especially shortness of breath, are primarily related to airway obstruction, and death is almost invariably due to asphyxiation (1). Increased airway responsiveness to provocative stimuli, termed airway hyperresponsiveness (AHR), and mucus hypersecretion by goblet cells are two of the principal causes of airway obstruction observed in asthma patients (2). Data from animal models consistently reveal a critical role for TH2 (T helper 2) cells and potentially important roles for the cytokines IL-4 and IL-5 (3-7).

TH2 cells selectively develop and expand in the presence of IL-4 (8). To separate direct effects of IL-4 from developmental effects on TH2 cells in an asthma model, we compared the ability to establish the asthma phenotype in BALB/c mice deficient in either IL-4 or the IL-4 receptor alpha  chain (IL-4Ralpha ) (9). After intranasal challenge with the antigen ovalbumin (OVA), BALB/c mice developed a stereotyped asthma phenotype characterized by eosinophil influx of the airways, goblet cell metaplasia with mucus overproduction, and an increase in AHR as revealed by enhanced sensitivity to acetylcholine challenge (6, 7). IL-4 and IL-4Ralpha -deficient mice showed incremental attenuation of each of these asthma indices (Fig. 1, C through E) (10). Thus, in agreement with prior studies (5-7), IL-4 contributes to the asthma phenotype, but these data suggest an independently greater contribution by IL-4Ralpha .

Fig. 1. PAS-stained histologic sections of murine lungs. Arrowheads point to goblet cells within the respiratory epithelium. (A) Wild-type mice were primed with OVA and challenged with PBS intranasally. (B) Wild-type mice were administered IL-13 intranasally. (C) IL-4-deficient and (D) IL-4Ralpha -deficient mice were primed with OVA and challenged with OVA intranasally. Wild-type mice were primed with OVA and challenged intranasally with (E) OVA and human Fc control protein or with (F) OVA and IL-13R-Fc. Note the marked reduction in goblet cells in (D) and (F). [View Larger Version of this Image (65K GIF file)]

IL-13 is a cytokine closely related to IL-4 that binds to IL-4Ralpha and is also expressed by TH2 cells from asthma patients (11). To assess whether IL-13 might contribute to the asthma phenotype, we administered a soluble IL-13 recetor alpha 2-human Fc fusion protein (IL-13R-Fc) to BALB/c mice sensitized to OVA and compared them to mice that received control protein (12). IL-13R-Fc selectively binds to and neutralizes murine IL-13 but not IL-4 (13). This treatment significantly attenuated the asthma phenotype, although little effect was seen on neutrophil influx into bronchoalveloar lavage (BAL) (Figs. 1, E and F, and 2). Thus, IL-13, like IL-4 (5-7), can contribute to the acute effector phase of experimental asthma.

Fig. 2. Effect of neutralization of IL-13. Primed wild-type mice were administered intranasally human immunoglobulin (Ig control), Ig control and OVA, or IL-13R-Fc and OVA as indicated by (+). Data for (A) AHR, (B) goblet cell score, and numbers of (C) eosinophils and (D) neutrophils in the BAL fluid are plotted as means ±SEM. *P < 0.05 relative to PBS and Ig control-treated mice; †P < 0.05 relative to OVA and Ig control-treated mice. Data are representative of at least two comparable experiments with four to eight mice per group. [View Larger Version of this Image (30K GIF file)]

To assess the capacity of IL-13 and IL-4 to cause pathology independently of T and B cells, we administered each cytokine to nonimmunized BALB/c and RAG1 (recombinase activating gene 1)-deficient mice (14). Each cytokine alone induced the asthma phenotype (Figs. 1, A and B, and 3). In contrast, administration of either cytokine to IL-4Ralpha -deficient mice resulted in no significant changes in any asthma parameter, demonstrating that their effects were dependent on signals mediated by IL-4Ralpha . Further, adoptive transfer of OVA-specific TH2 cells to IL-4Ralpha -deficient mice failed to elicit the asthma phenotype, whereas identical treatment of wild-type mice resulted in the full phenotype (15, 16). Thus, experimental asthma induced by antigen challenge, recombinant cytokine, or adoptive transfer of TH2 cells, is mediated through a final pathway dependent on IL-4Ralpha .

Fig. 3. Effect of recombinant IL-4 and IL-13. Wild-type (WT), RAG1-deficient (RAG1-/-), and IL-4Ralpha -deficient (IL-4Ralpha -/-) mice were administered IL-4, IL-13, or control protein intranasally. Data for (A) AHR, (B) goblet cell score, and numbers of (C) eosinophils and (D) neutrophils in the BAL fluid are plotted as means ±SEM. *P < 0.05 relative to mice receiving control protein. Data are representative of at least two comparable experiments with four to eight mice per group. [View Larger Version of this Image (45K GIF file)]

Attenuated asthma phenotypes observed in IL-4-deficient mice may now be interpreted as representing the effects of residual IL-13 derived from IL-4-deficient TH2 cells (17). Parallel observations in experimental intestinal helminth infections demonstrate roles for both IL-4 and IL-13 in mediating critical final effector pathways via IL-4Ralpha (18). It is possible that human asthma represents a spectrum of disease also linked by a shared receptor effector pathway. The common embryological origin of tissues from the gut and lung (19) would support the presence of stereotyped responses in these organs.

The relevance of our data to human asthma remains an important issue that cannot be entirely addressed, given the complexity of the disease and the inadequacies of any animal model. Linkage analysis has mapped susceptibility to asthma to a region on human chromosome 5q25-31, which includes the genes for both IL-4 and IL-13 (20), and to mutations in two domains of the alpha  chain of the IL-4 receptor (21). A number of additional regions in the genome have been linked to asthma in human studies, suggesting a complex multifactorial phenotype (22). As we suggest, however, diverse forms of asthma might follow a final common effector pathway mediated through signals transduced by IL-4Ralpha , thus creating a unified target for potential intervention.

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3 September 1998; accepted 4 November 1998


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   Abstract »    Full Text »    PDF »
Evidence That CD8+ Dendritic Cells Enable the Development of {gamma}{delta} T Cells That Modulate Airway Hyperresponsiveness.
L. Cook, N. Miyahara, N. Jin, J. M. Wands, C. Taube, C. L. Roark, T. A. Potter, E. W. Gelfand, R. L. O'Brien, and W. K. Born (2008)
J. Immunol. 181, 309-319
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Interleukin-4 activates large-conductance, calcium-activated potassium (BKCa) channels in human airway smooth muscle cells.
G. Martin, R. J. O'Connell, A. Z. Pietrzykowski, S. N. Treistman, M. F. Ethier, and J. M. Madison (2008)
Exp Physiol 93, 908-918
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Strain-specific requirement for eosinophils in the recruitment of T cells to the lung during the development of allergic asthma.
E. R. Walsh, N. Sahu, J. Kearley, E. Benjamin, B. H. Kang, A. Humbles, and A. August (2008)
J. Exp. Med. 205, 1285-1292
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Interleukin-13 Neutralization by Two Distinct Receptor Blocking Mechanisms Reduces Immunoglobulin E Responses and Lung Inflammation in Cynomolgus Monkeys.
M. T. Kasaian, X.-Y. Tan, M. Jin, L. Fitz, K. Marquette, N. Wood, T. A. Cook, J. Lee, A. Widom, R. Agostinelli, et al. (2008)
J. Pharmacol. Exp. Ther. 325, 882-892
   Abstract »    Full Text »    PDF »
Distinct roles for IL-13 and IL-4 via IL-13 receptor {alpha}1 and the type II IL-4 receptor in asthma pathogenesis.
A. Munitz, E. B. Brandt, M. Mingler, F. D. Finkelman, and M. E. Rothenberg (2008)
PNAS 105, 7240-7245
   Abstract »    Full Text »    PDF »
Lung Lining Fluid Glutathione Attenuates IL-13-Induced Asthma.
M. H. Lowry, B. P. McAllister, J.-C. Jean, L. A. S. Brown, R. P. Hughey, W. W. Cruikshank, S. Amar, E. C. Lucey, K. Braun, P. Johnson, et al. (2008)
Am. J. Respir. Cell Mol. Biol. 38, 509-516
   Abstract »    Full Text »    PDF »
Identification of Pendrin as a Common Mediator for Mucus Production in Bronchial Asthma and Chronic Obstructive Pulmonary Disease.
I. Nakao, S. Kanaji, S. Ohta, H. Matsushita, K. Arima, N. Yuyama, M. Yamaya, K. Nakayama, H. Kubo, M. Watanabe, et al. (2008)
J. Immunol. 180, 6262-6269
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Nuclear Factor-{kappa}B Activation in Airway Epithelium Induces Inflammation and Hyperresponsiveness.
C. Pantano, J. L. Ather, J. F. Alcorn, M. E. Poynter, A. L. Brown, A. S. Guala, S. L. Beuschel, G. B. Allen, L. A. Whittaker, M. Bevelander, et al. (2008)
Am. J. Respir. Crit. Care Med. 177, 959-969
   Abstract »    Full Text »    PDF »
Interleukin 13 Increases Contractility of Murine Tracheal Smooth Muscle by a Phosphoinositide 3-kinase p110{delta}-Dependent Mechanism.
H. S. M. Farghaly, I. S. Blagbrough, D. A. Medina-Tato, and M. L. Watson (2008)
Mol. Pharmacol. 73, 1530-1537
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Mast cell-derived tumour necrosis factor is essential for allergic airway disease.
S. Reuter, A. Heinz, M. Sieren, R. Wiewrodt, E. W. Gelfand, M. Stassen, R. Buhl, and C. Taube (2008)
Eur. Respir. J. 31, 773-782
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Development of Chronic Bronchitis and Emphysema in {beta}-Epithelial Na+ Channel-Overexpressing Mice.
M. A. Mall, J. R. Harkema, J. B. Trojanek, D. Treis, A. Livraghi, S. Schubert, Z. Zhou, S. M. Kreda, S. L. Tilley, E. J. Hudson, et al. (2008)
Am. J. Respir. Crit. Care Med. 177, 730-742
   Abstract »    Full Text »    PDF »
Dual Modulation of Airway Smooth Muscle Contraction by Th2 Cytokines via Matrix Metalloproteinase-1 Production.
Y. Ohta, M. Hayashi, T. Kanemaru, K. Abe, Y. Ito, and M. Oike (2008)
J. Immunol. 180, 4191-4199
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IL-9 and IL-13 Induce Mucous Cell Metaplasia That Is Reduced by IFN-{gamma} in a Bax-Mediated Pathway.
J. Xiang, J. Rir-Sim-Ah, and Y. Tesfaigzi (2008)
Am. J. Respir. Cell Mol. Biol. 38, 310-317
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IL-4 Is a Critical Determinant in the Generation of Allergic Inflammation Initiated by a Constitutively Active Stat6.
S. Sehra, H. A. Bruns, A.-N. N. Ahyi, E. T. Nguyen, N. W. Schmidt, E. G. Michels, G.-U. von Bulow, and M. H. Kaplan (2008)
J. Immunol. 180, 3551-3559
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Murine Cytomegalovirus Influences Foxj1 Expression, Ciliogenesis, and Mucus Plugging in Mice with Allergic Airway Disease.
C. A. Wu, J. J. Peluso, J. D. Shanley, L. Puddington, and R. S. Thrall (2008)
Am. J. Pathol. 172, 714-724
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Pulmonary arterial remodeling induced by a Th2 immune response.
E. Daley, C. Emson, C. Guignabert, R. de Waal Malefyt, J. Louten, V. P. Kurup, C. Hogaboam, L. Taraseviciene-Stewart, N. F. Voelkel, M. Rabinovitch, et al. (2008)
J. Exp. Med. 205, 361-372
   Abstract »    Full Text »    PDF »
Chlamydia muridarum Infection Subverts Dendritic Cell Function to Promote Th2 Immunity and Airways Hyperreactivity.
G. E. Kaiko, S. Phipps, D. K. Hickey, C. E. Lam, P. M. Hansbro, P. S. Foster, and K. W. Beagley (2008)
J. Immunol. 180, 2225-2232
   Abstract »    Full Text »    PDF »
Gene Expression in Asthmatic Airway Smooth Muscle.
P. G. Woodruff (2008)
Proceedings of the ATS 5, 113-118
   Abstract »    Full Text »    PDF »
IL-13 Receptor {alpha}2 Selectively Inhibits IL-13-Induced Responses in the Murine Lung.
T. Zheng, W. Liu, S.-Y. Oh, Z. Zhu, B. Hu, R. J. Homer, L. Cohn, M. J. Grusby, and J. A. Elias (2008)
J. Immunol. 180, 522-529
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Interaction between GATA-3 and the Transcriptional Coregulator Pias1 Is Important for the Regulation of Th2 Immune Responses.
X. Zhao, B. Zheng, Y. Huang, D. Yang, S. Katzman, C. Chang, D. Fowell, and W.-p. Zeng (2007)
J. Immunol. 179, 8297-8304
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Anti-inflammatory and Immune-regulatory Effects of Subcutaneous Perillae Fructus Extract Injections on OVA-induced Asthma in Mice.
Y.-K. Yim, H. Lee, K.-E. Hong, Y.-I. Kim, S.-K. Ko, J.-E. Kim, S.-Y. Lee, and K.-S. Park (2007)
Evid. Based Complement. Altern. Med.
   Abstract »    Full Text »    PDF »
Genetics of Asthma: Potential Implications for Reducing Asthma Disparities.
C. V. Scirica and J. C. Celedon (2007)
Chest 132, 770S-781S
   Abstract »    Full Text »    PDF »
IL-13 Induces Disease-Promoting Type 2 Cytokines, Alternatively Activated Macrophages and Allergic Inflammation during Pulmonary Infection of Mice with Cryptococcus neoformans.
U. Muller, W. Stenzel, G. Kohler, C. Werner, T. Polte, G. Hansen, N. Schutze, R. K. Straubinger, M. Blessing, A. N. J. McKenzie, et al. (2007)
J. Immunol. 179, 5367-5377
   Abstract »    Full Text »    PDF »
The Immunopathogenesis of Chronic Obstructive Pulmonary Disease: Insights from Recent Research.
J. L. Curtis, C. M. Freeman, and J. C. Hogg (2007)
Proceedings of the ATS 4, 512-521
   Abstract »    Full Text »    PDF »
Allergic Airway Responses in Obese Mice.
R. A. Johnston, M. Zhu, Y. M. Rivera-Sanchez, F. L. Lu, T. A. Theman, L. Flynt, and S. A. Shore (2007)
Am. J. Respir. Crit. Care Med. 176, 650-658
   Abstract »    Full Text »    PDF »
Neonatal Chlamydial Infection Induces Mixed T-Cell Responses That Drive Allergic Airway Disease.
J. C. Horvat, K. W. Beagley, M. A. Wade, J. A. Preston, N. G. Hansbro, D. K. Hickey, G. E. Kaiko, P. G. Gibson, P. S. Foster, and P. M. Hansbro (2007)
Am. J. Respir. Crit. Care Med. 176, 556-564
   Abstract »    Full Text »    PDF »
T helper 1 cells stimulated with ovalbumin and IL-18 induce airway hyperresponsiveness and lung fibrosis by IFN-{gamma} and IL-13 production.
N. Hayashi, T. Yoshimoto, K. Izuhara, K. Matsui, T. Tanaka, and K. Nakanishi (2007)
PNAS 104, 14765-14770
   Abstract »    Full Text »    PDF »
CD8+ T Cell-Mediated Airway Hyperresponsiveness and Inflammation Is Dependent on CD4+IL-4+ T Cells.
T. Koya, N. Miyahara, K. Takeda, S. Matsubara, H. Matsuda, C. Swasey, A. Balhorn, A. Dakhama, and E. W. Gelfand (2007)
J. Immunol. 179, 2787-2796
   Abstract »    Full Text »    PDF »
Inhibition of Experimental Allergic Airways Disease by Local Application of a Cell-Penetrating Dominant-Negative STAT-6 Peptide.
C. T. McCusker, Y. Wang, J. Shan, M. W. Kinyanjui, A. Villeneuve, H. Michael, and E. D. Fixman (2007)
J. Immunol. 179, 2556-2564
   Abstract »    Full Text »    PDF »
The Early Growth Response Factor-1 Is Involved in Stem Cell Factor (SCF)-induced Interleukin 13 Production by Mast Cells, but Is Dispensable for SCF-dependent Mast Cell Growth.
B. Li, J. Berman, J.-T. Tang, and T.-J. Lin (2007)
J. Biol. Chem. 282, 22573-22581
   Abstract »    Full Text »    PDF »
T-cell co-stimulatory molecules: novel targets for the treatment of allergic airway disease.
K. C. Beier, T. Kallinich, and E. Hamelmann (2007)
Eur. Respir. J. 30, 383-390
   Abstract »    Full Text »    PDF »
Coordinated Involvement of Mast Cells and T Cells in Allergic Mucosal Inflammation: Critical Role of the CC Chemokine Ligand 1:CCR8 Axis.
J.-A. Gonzalo, Y. Qiu, J. M. Lora, A. Al-Garawi, J.-L. Villeval, J. A. Boyce, C. Martinez-A, G. Marquez, I. Goya, Q. Hamid, et al. (2007)
J. Immunol. 179, 1740-1750
   Abstract »    Full Text »    PDF »
Measurement of IL-13-Induced iNOS-Derived Gas Phase Nitric Oxide in Human Bronchial Epithelial Cells.
V. Suresh, J. D. Mih, and S. C. George (2007)
Am. J. Respir. Cell Mol. Biol. 37, 97-104
   Abstract »    Full Text »    PDF »
Galectin-9 Inhibits CD44-Hyaluronan Interaction and Suppresses a Murine Model of Allergic Asthma.
S. Katoh, N. Ishii, A. Nobumoto, K. Takeshita, S.-Y. Dai, R. Shinonaga, T. Niki, N. Nishi, A. Tominaga, A. Yamauchi, et al. (2007)
Am. J. Respir. Crit. Care Med. 176, 27-35
   Abstract »    Full Text »    PDF »
Complement C3a Regulates Muc5ac Expression by Airway Clara Cells Independently of Th2 Responses.
P. Dillard, R. A. Wetsel, and S. M. Drouin (2007)
Am. J. Respir. Crit. Care Med. 175, 1250-1258
   Abstract »    Full Text »    PDF »
T-cell co-stimulatory molecules: their role in allergic immune reactions.
T. Kallinich, K. C. Beier, U. Wahn, P. Stock, and E. Hamelmann (2007)
Eur. Respir. J. 29, 1246-1255
   Abstract »    Full Text »    PDF »
4-1BB triggers IL-13 production from T cells to limit the polarized, Th1-mediated inflammation.
S. M. Shin, Y. H. Kim, B. K. Choi, P. M. Kwon, H.-W. Lee, and B. S. Kwon (2007)
J. Leukoc. Biol. 81, 1455-1465
   Abstract »    Full Text »    PDF »
Molecular Characterization of Inflammatory Genes in Sentinel and Nonsentinel Nodes in Melanoma.
H. Torisu-Itakura, J. H. Lee, R. P. Scheri, Y. Huynh, X. Ye, R. Essner, and D. L. Morton (2007)
Clin. Cancer Res. 13, 3125-3132
   Abstract »    Full Text »    PDF »
Ethnicity-specific Gene-Gene Interaction between IL-13 and IL-4R{alpha} among African Americans with Asthma.
N. C. Battle, S. Choudhry, H.-J. Tsai, C. Eng, G. Kumar, K. B. Beckman, M. Naqvi, K. Meade, H. G. Watson, M. LeNoir, et al. (2007)
Am. J. Respir. Crit. Care Med. 175, 881-887
   Abstract »    Full Text »    PDF »
Airway Exposure Levels of Lipopolysaccharide Determine Type 1 versus Type 2 Experimental Asthma.
Y.-K. Kim, S.-Y. Oh, S. G. Jeon, H.-W. Park, S.-Y. Lee, E.-Y. Chun, B. Bang, H.-S. Lee, M.-H. Oh, Y.-S. Kim, et al. (2007)
J. Immunol. 178, 5375-5382
   Abstract »    Full Text »    PDF »
Lysophosphatidic Acid Induces Interleukin-13 (IL-13) Receptor {alpha}2 Expression and Inhibits IL-13 Signaling in Primary Human Bronchial Epithelial Cells.
Y. Zhao, D. He, J. Zhao, L. Wang, A. R. Leff, E. Wm. Spannhake, S. Georas, and V. Natarajan (2007)
J. Biol. Chem. 282, 10172-10179
   Abstract »    Full Text »    PDF »
Superantigen Presentation by Airway Smooth Muscle to CD4+ T Lymphocytes Elicits Reciprocal Proasthmatic Changes in Airway Function.
H. Veler, A. Hu, S. Fatma, J. S. Grunstein, C. M. DeStephan, D. Campbell, J. S. Orange, and M. M. Grunstein (2007)
J. Immunol. 178, 3627-3636
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Efficacy of IL-13 Neutralization in a Sheep Model of Experimental Asthma.
M. T. Kasaian, D. D. Donaldson, L. Tchistiakova, K. Marquette, X.-Y. Tan, A. Ahmed, B. A. Jacobson, A. Widom, T. A. Cook, X. Xu, et al. (2007)
Am. J. Respir. Cell Mol. Biol. 36, 368-376
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IL-13 Mediates In Vivo IL-9 Activities on Lung Epithelial Cells but Not on Hematopoietic Cells.
V. Steenwinckel, J. Louahed, C. Orabona, F. Huaux, G. Warnier, A. McKenzie, D. Lison, R. Levitt, and J.-C. Renauld (2007)
J. Immunol. 178, 3244-3251
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Functional Dissection Identifies a Conserved Noncoding Sequence-1 Core That Mediates IL13 and IL4 Transcriptional Enhancement.
J. M. Strempel and D. Vercelli (2007)
J. Biol. Chem. 282, 3738-3746
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IL-13 and Epidermal Growth Factor Receptor Have Critical but Distinct Roles in Epithelial Cell Mucin Production.
G. Zhen, S. W. Park, L. T. Nguyenvu, M. W. Rodriguez, R. Barbeau, A. C. Paquet, and D. J. Erle (2007)
Am. J. Respir. Cell Mol. Biol. 36, 244-253
   Abstract »    Full Text »    PDF »
Inducible expression of the proallergic cytokine thymic stromal lymphopoietin in airway epithelial cells is controlled by NF{kappa}B.
H.-C. Lee and S. F. Ziegler (2007)
PNAS 104, 914-919
   Abstract »    Full Text »    PDF »
The Human IL-13 Locus in Neonatal CD4+ T Cells Is Refractory to the Acquisition of a Repressive Chromatin Architecture.
R. B. Webster, Y. Rodriguez, W. T. Klimecki, and D. Vercelli (2007)
J. Biol. Chem. 282, 700-709
   Abstract »    Full Text »    PDF »
IL9 leads to airway inflammation by inducing IL13 expression in airway epithelial cells.
U.-A. Temann, Y. Laouar, E. E. Eynon, R. Homer, and R. A. Flavell (2007)
Int. Immunol. 19, 1-10
   Abstract »    Full Text »    PDF »
Effects of a Low-Molecular-Weight CCR-3 Antagonist on Chronic Experimental Asthma.
M. Wegmann, R. Goggel, S. Sel, S. Sel, K. J. Erb, F. Kalkbrenner, H. Renz, and H. Garn (2007)
Am. J. Respir. Cell Mol. Biol. 36, 61-67
   Abstract »    Full Text »    PDF »
Comparative Roles of IL-4, IL-13, and IL-4R{alpha} in Dendritic Cell Maturation and CD4+ Th2 Cell Function.
D. C. Webb, Y. Cai, K. I. Matthaei, and P. S. Foster (2007)
J. Immunol. 178, 219-227
   Abstract »    Full Text »    PDF »
Antenatal risk factors, cytokines and the development of atopic disease in early childhood.
E K Chung, R L Miller, M T Wilson, S J McGeady, and J F Culhane (2007)
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
   Abstract »    Full Text »    PDF »
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
   Abstract »    Full Text »    PDF »
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
   Abstract »    Full Text »    PDF »
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
   Abstract »    Full Text »    PDF »
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
   Abstract »    Full Text »    PDF »
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
   Abstract »    Full Text »    PDF »


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