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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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The role of T lymphocytes in the pathogenesis of asthma

TL;DR: The efficacy of cyclosporin A and anti-CD4 treatment in patients with chronic severe asthma argues for continued T-cell involvement, but whether remodeling contributes to pathology inaccessible to anti-inflammatory treatment or T- cell immunotherapy will be an important future question.
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Cytokines in chronic obstructive pulmonary disease

TL;DR: The cytokine profile seen in chronic obstructive pulmonary disease is different from that observed in asthma, and the role of these cytokines needs to be defined and there is a potential for anticytokine therapy in chronic obstetric pulmonary disease.

Mucosal immunity relies on the delicate balance between antigen responsiveness and tolerance. The polarization of T helper cells plays a key role in maintaining or disrupting this equilibrium. The role of Th1/Th2 polarization in mucosal immunity

TL;DR: Mucosal immunity relies on the delicate balance between antigen responsiveness and tolerance and the polarization of T helper cells plays a key role in maintaining this equilibrium.
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IL-13 receptors and signaling pathways: An evolving web

TL;DR: The current understanding of the IL-13 receptors and signaling pathways is summarized, supported by many in vivo observations, including that administration ofIL-13 resulted in allergic inflammation, tissue-specific overexpression of IL- 13 in the lungs of transgenic mice resulted in airway inflammation and mucus hypersecretion.
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Stimulation of Airway Mucin Gene Expression by Interleukin (IL)-17 through IL-6 Paracrine/Autocrine Loop

TL;DR: Investigation of MUC5B expression demonstrated that IL-17's effect is at least partly mediated through IL-6 by a JAK2-dependent autocrine/paracrine loop, and evidence is presented to show that both IL-4, IL-9, and IL-13 mediate Muc5Bexpression through the ERK signaling pathway.
References
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Journal ArticleDOI

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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.
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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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