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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

A dual activation and inhibition role for the paired immunoglobulin-like receptor B in eosinophils.

TL;DR: PIR-B was up-regulated in an eosinophil-dependent manner in the lungs of allergen-challenged and interleukin (IL)-13-overexpressing mice and it is proposed that a single receptor can have dual functionality in distinct cell types after unique cellular signals.
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The contribution of toll-like receptors to the pathogenesis of asthma

TL;DR: The cellular distribution of TLR in the lung and their potential contribution to the processes that promote T helper 2 (Th2) immunity and infection‐induced exacerbations of allergic lung disease are reviewed.
Journal ArticleDOI

A phase 1, randomized, placebo‐controlled, dose‐escalation study of an anti‐IL‐13 monoclonal antibody in healthy subjects and mild asthmatics

TL;DR: GSK679586 demonstrated dose-dependent pharmacological activity in the lungs of mild intermittent asthmatics, together with the favourable safety profile and advantageous PK characteristics of a monoclonal antibody, warrant further investigation of GSK679585 in a broader asthma patient population.
Journal ArticleDOI

Lipoxin B4 promotes the resolution of allergic inflammation in the upper and lower airways of mice

TL;DR: It is indicated that LXB4 carries cell type selective and mucosal protective actions that broaden the lipoxin family’s therapeutic potential for upper and lower airway catabasis.
Journal ArticleDOI

TGF-beta, eosinophils and IL-13 in allergic airway remodeling: a critical appraisal with therapeutic considerations.

TL;DR: The evidence pertaining to the roles of TGF-beta, eosinophils and IL-13 in allergic remodeling is appraised, and it is suggested that identifying robust targets for therapeutic intervention might benefit from a reconsideration of the approach to understanding remodeling.
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.
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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.
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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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