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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

Eosinophilic and neutrophilic inflammation in asthma: insights from clinical studies.

TL;DR: New insights about the relationships between cellular inflammation and disease phenotypes of asthma support the concept that different subgroups of patients with asthma, despite clinically similar features, can be defined by specific cellular and molecular markers.
Journal ArticleDOI

A Role for Immune Complexes in Enhanced Respiratory Syncytial Virus Disease

TL;DR: It is demonstrated that enhanced RSV disease is mediated by immune complexes and abrogated in complement component C3 and B cell–deficient mice but not in controls, and correlation with the enhanced disease observed in children is shown by providing evidence of complement activation in postmortem lung sections from children with enhancedRSV disease.
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Pathology of asthma

TL;DR: Asthma is classically recognized as the typical Th2 disease, with increased IgE levels and eosinophilic inflammation in the airway, which induces airway remodeling and induces increased airway smooth muscle mass, which generate asthmatic symptoms.
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Simultaneous disruption of interleukin (IL)-4 and IL-13 defines individual roles in T helper cell type 2-mediated responses.

TL;DR: It is concluded that IL-4 and IL-13 cooperate to initiate rapid Th2 cell–driven responses, and that although their functions overlap, they perform additive roles.
References
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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.
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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