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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Book ChapterDOI
T cell effector subsets: extending the Th1/Th2 paradigm.
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Acute and chronic airway responses to viral infection: implications for asthma and chronic obstructive pulmonary disease.
Michael J. Holtzman,Jeffrey W. Tyner,Edy Y. Kim,Mindy S. Lo,Anand C. Patel,Laurie P. Shornick,Eugene Agapov,Yong Zhang +7 more
TL;DR: Using a mouse model of viral bronchiolitis, it is found that antiviral defense depends at least in part on a network of mucosal epithelial cells and macrophages specially programmed for immune-response gene expression, and identifying specific components of the mucosal immune system that manifest an aberrant antiviral response may allow for adjusting this response to improve acute and chronic outcomes after viral infection.
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Enhanced airway inflammation and decreased subepithelial fibrosis in interleukin 6-deficient mice following chronic exposure to aerosolized antigen.
TL;DR: Airway inflammation and remodelling are characteristic features of chronic asthma and are a cause of concern in patients with asthma.
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IL-13 Fusion Cytotoxin Ameliorates Chronic Fungal-Induced Allergic Airway Disease in Mice
TL;DR: It is demonstrated that a therapy designed to target IL-13-responsive cells in the lung ameliorates established fungal-induced allergic airway disease in mice.
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Exacerbated Th2-mediated airway inflammation and hyperresponsiveness in autoimmune diabetes-prone NOD mice: a critical role for CD1d-dependent NKT cells.
Luiza M Araujo,Jean Lefort,Marie-Anne Nahori,Séverine Diem,Ren Zhu,Michel Dy,Maria Leite-de-Moraes,Jean Francois Bach,B Boris Vargaftig,André Herbelin +9 more
TL;DR: It is shown that NOD mice have the capacity to develop a typical Th2‐mediated disease, namely experimental allergic asthma, and these hallmarks of allergic asthma were associated with increased IL‐4,IL‐5, IL‐13 and eotaxin production in the lungs, as compared with BALB/c mice.
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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.
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