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Open AccessJournal Article

Interleukin-13: Central mediator of allergic asthma

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.

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Citations
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Induction of allergic inflammation by interleukin-18 in experimental animal models.

TL;DR: Interleukin‐18 (IL‐18) has been regarded as a proinflammatory cytokine because of its potent interferon‐γ‐inducing activity, but mutant mice that release excess amounts of IL‐18 spontaneously develop pruritic chronic dermatitis‐like atopic dermatitis (AD), suggesting the importance of IL-18 for the development of AD.
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Novel dinucleotide repeat polymorphism in the first exon of the STAT-6 gene is associated with allergic diseases

TL;DR: Background T helper‐type 2 cytokines, such as interleukin‐4 (IL‐4) and IL‐13, may play a central role in allergic diseases andSTAT‐6 is a key transcription factor involved in both IL‐4‐ and IL-13‐mediated biological responses.
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Dissociation of inflammatory and epithelial responses in a murine model of chronic asthma.

TL;DR: It is concluded that interleukin-5, but not interleucin-4, plays a central role in the development of chronic inflammation of the airways and the induction of airway hyperreactivity.
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Asthmatic changes in mice lacking T-bet are mediated by IL-13.

TL;DR: Interestingly, neutralization of TGF-beta ameliorated aspects of the chronic airway remodeling phenotype but did not reduce AHR, highlighting a T-bet-directed function for IL-13 in controlling lung remodeling that is both dependent on and independent of its interaction with T GF-beta in the asthmatic airway.
Journal ArticleDOI

Neuroimmunology of the Interleukins 13 and 4.

TL;DR: In mice and man, the gene encoding for IL-13Rα1 is expressed on the X chromosome within the PARK12 region of susceptibility to Parkinson’s disease (PD), indicating the possibility that these cytokines may contribute to the etiology or the progression of PD.
References
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TL;DR: The existence of subsets of CD4+ helper T lymphocytes that differ in their cytokine secretion patterns and effector functions provides a framework for understanding the heterogeneity of normal and pathological immune responses.
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Predominant TH2-like bronchoalveolar T-lymphocyte population in atopic asthma

TL;DR: Atopic asthma is associated with activation in the bronchi of the interleukin-3, 4, and 5 and GM-CSF gene cluster, a pattern compatible with predominant activation of the TH2-like T-cell population.
Journal ArticleDOI

Eosinophilic inflammation in asthma.

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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Requirement for IL-13 Independently of IL-4 in Experimental Asthma

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

Cellular events in the bronchi in mild asthma and after bronchial provocation.

TL;DR: It is concluded that allergic asthma is accompanied by extensive inflammatory changes in the airways, even in mild clinical and subclinical disease.
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