Open AccessJournal Article
Interleukin-13: Central mediator of allergic asthma
Marsha Wills-Karp,Jackie Luyimbazi,Xueying Xu,Brian Schofield,Tamlyn Neben,Christopher L. Karp,Debra D. Donaldson +6 more
TLDR
In this article, 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.Abstract:
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.read more
Citations
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Airway mucus, inflammation and remodeling: emerging links in the pathogenesis of chronic lung diseases.
TL;DR: These studies confirm that mucus hyperconcentration on airway surfaces plays a critical role in the pathophysiology of impaired MCC, mucus adhesion and airway plugging that cause airflow obstruction and provide a nidus for bacterial infection and suggest that improvement of mucus clearance may be a promising therapeutic strategy for a spectrum of muco-obstructive lung diseases.
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Insights into the pathogenesis of asthma utilizing murine models.
TL;DR: To further understand this complex syndrome, the development of animal models which mimic elements of this chronic airway disease is essential.
Journal ArticleDOI
Eosinophil Major Basic Protein-1 Does Not Contribute to Allergen-Induced Airway Pathologies in Mouse Models of Asthma
Karen L. Denzler,S. Farmer,Jeffrey R. Crosby,Michael T. Borchers,G Cieslewicz,Kirsten A. Larson,Stephania Cormier-Regard,Nancy A. Lee,James J. Lee +8 more
TL;DR: The relationship between eosinophils and the development of Ag-induced pulmonary pathologies, including airway hyper-responsiveness, was investigated using mice deficient for the secondary granule component, major basic protein-1 (mMBP-1).
Journal ArticleDOI
Kinetic analysis of the interleukin-13 receptor complex.
Allison-Lynn Andrews,John W. Holloway,Sarah M. Puddicombe,Stephen T. Holgate,Donna E. Davies +4 more
TL;DR: Kinetic analyses of the binding properties of the heteromeric complexes suggested a sequential mechanism for the binding of IL-13 to its signaling receptor, in whichIL-13 first binds to IL- 13Rα1 and this then recruits IL-4Rα to stabilize a high affinity interaction.
Journal ArticleDOI
Pulmonary Chemokine Expression Is Coordinately Regulated by STAT1, STAT6, and IFN-γ
TL;DR: It is demonstrated that allergen-induced inflammation involves coordinate regulation by STAT1, STAT6, and IFN-γ, and only a select panel of chemokines (those targeting Th2 cells and eosinophils) is positively regulated by STAT6.
References
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TL;DR: Eosinophilic inflammation of the airways is correlated with the severity of asthma and these cells are likely to play a part in the epithelial damage seen in this disease.
Journal ArticleDOI
Requirement for IL-13 Independently of IL-4 in Experimental Asthma
Gabriele Grünig,Martha L. Warnock,Adil E. Wakil,Rajeev Venkayya,Frank Brombacher,Donna M. Rennick,Dean Sheppard,Markus Mohrs,Debra D. Donaldson,Richard M. Locksley,David B. Corry +10 more
TL;DR: This article showed that IL-4 receptor α chain-dependent pathway may underlie the genetic associations of asthma with both the human 5q31 locus and the IL4 receptor and showed that selective neutralization of IL-13, a cytokine related to interleukin-4 that also binds to the α chain of the IL 4 receptor, ameliorated asthma phenotype.
Journal ArticleDOI
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