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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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Book ChapterDOI

Regulation of IL-4 Expression in Immunity and Diseases.

TL;DR: This chapter will review in detail the molecular mechanism regulating the cell type-specific expression of IL-4 in physiological and pathological type 2 immune responses.
Journal ArticleDOI

Targeting IL-4/IL-13 signaling to alleviate oral allergen–induced diarrhea

TL;DR: Endogenously produced IL-13 supplements the ability of IL-4 to induce allergic diarrhea by promoting oral allergen sensitization rather than the effector phase of intestinal anaphylaxis.
Journal ArticleDOI

An open-label, single-dose bioavailability study of the pharmacokinetics of CAT-354 after subcutaneous and intravenous administration in healthy males

TL;DR: CAT-354 exhibited bioavailability of approximately 60% when given s.c. to healthy male subjects, and dosing was consistent with endogenous IgG and reticuloendothelial elimination.
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Mycoplasma pneumoniae induces host-dependent pulmonary inflammation and airway obstruction in mice.

TL;DR: The mice in this study exhibited host-dependent infection-related AO and AHR associated with chemokine and T-helper type (Th)1 pulmonary host response and not Th2 response after M. pneumoniae infection.
Journal ArticleDOI

Eosinophil trafficking in asthma.

TL;DR: The implications of this multistep process are that antagonists of IL-5, VLA-4, PSGL-1 and CC chemokine receptor 3, as well as IL-4 and IL-13, each have the potential markedly to inhibit eosinophil recruitment in asthma.
References
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Predominant TH2-like bronchoalveolar T-lymphocyte population in atopic asthma

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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.
Journal ArticleDOI

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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