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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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A phase II placebo-controlled study of tralokinumab in moderate-to-severe asthma

TL;DR: The effects of tralokinumab, an investigational human IL-13-neutralising immunoglobulin G4 monoclonal antibody, in adults with moderate-to-severe uncontrolled asthma despite controller therapies was assessed, although no improvement in ACQ-6 was observed, although tralokerumab treatment was associated with improved lung function.
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Taking our breath away: dendritic cells in the pathogenesis of asthma.

TL;DR: It is proposed that DCs are similarly essential for controlling effector T-cell responses and, therefore, might have a role in T- cell-mediated diseases.
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Defective lipoxin-mediated anti-inflammatory activity in the cystic fibrosis airway.

TL;DR: It is reported here that lipoxin concentrations in airway fluid were significantly suppressed in patients with cystic fibrosis compared to patients with other inflammatory lung conditions and that lipoxins have therapeutic potential in this lethal autosomal disease.
Journal ArticleDOI

Protectin D1 Is Generated in Asthma and Dampens Airway Inflammation and Hyperresponsiveness

TL;DR: Findings provide evidence for endogenous PD1 as a pivotal counterregulatory signal in allergic airway inflammation and point to new therapeutic strategies for modulating inflammation in asthmatic lung.
Journal ArticleDOI

IL-4 and IL-13 signaling in allergic airway disease.

TL;DR: The purpose of this chapter is to review the current understanding of the distinct roles that IL-4 and IL-13 play in allergic inflammatory states and the utility of their modulation as potential therapeutic strategies for the treatment of allergic disorders.
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.
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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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