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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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Journal ArticleDOI

Role of IL-6 in asthma and other inflammatory pulmonary diseases.

TL;DR: An overview of the studies in mouse models and human patients that provide support for the involvement of IL-6 in lung diseases is provided and suggests that this cytokine plays an active role in pathogenesis of asthma and, in all likelihood, COPD.
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Innate IL-13–producing nuocytes arise during allergic lung inflammation and contribute to airways hyperreactivity

TL;DR: These findings identify nuocytes as a novel cell type in allergic lung inflammation and an innate source of IL-13 that can directly induce AHR in the absence ofIL-13-producing CD4(+) T cells.
Journal ArticleDOI

Cytokines in asthma

TL;DR: In vivo animal data suggest a sequential involvement of interleukin (IL)‐4 and IL‐5 in the induction of allergen-induced airway changes and that T‐cell-derived cytokine production, rather than eosinophil influx or immunoglobulin‐E synthesis, is causally related to altered airway behaviour.
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Efficacy of soluble IL-4 receptor for the treatment of adults with asthma

TL;DR: These promising data suggest that IL-4R is safe and effective in the treatment of moderate persistent asthma.
Journal ArticleDOI

Critical role for IL-13 in the development of allergen-induced airway hyperreactivity.

TL;DR: It is definitively demonstrate that IL-13 is necessary and sufficient for the induction of AHR and that eosinophilic airway inflammation in the absence of IL- 13 is inadequate for the induction of A HR, and treatment of human asthma with antagonists ofIL-13 may be very effective.
References
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Journal ArticleDOI

Functional diversity of helper T lymphocytes.

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.
Journal ArticleDOI

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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