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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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Effects of omalizumab on markers of inflammation in patients with allergic asthma.

TL;DR: The anti‐inflammatory effects of omalizumab may explain the reductions in asthma exacerbations and symptoms seen in clinical trials in patients with moderate‐to‐severe or severe, persistent, inadequately controlled allergic asthma.
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Targeting Interleukin-4 in Asthma: Lost in Translation?

TL;DR: The role of IL-4 in asthma,IL-4 signaling, which is crucial in the development of allergic airway inflammation, is addressed, and an overview of preclinical and clinical studies targeting the IL- 4 Receptor pathway is given.
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Immune markers in breast milk and fetal and maternal body fluids: a systematic review of perinatal concentrations.

TL;DR: In this paper, a PubMed search was conducted to review studies in humans and analyze concentrations of immune markers found in maternal serum, amniotic fluid, cord serum, colostrum, transition and mature milk.
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Allergen-induced Increases in Sputum Levels of Group 2 Innate Lymphoid Cells in Subjects with Asthma.

TL;DR: Innate and adaptive immune cells are increased in the airways associated with allergic asthmatic responses, and total and type 2 cytokine‐positive ILC2 are increased only within the airway, whereas CD4+ T lymphocytes demonstrated local and systemic increases.
Journal ArticleDOI

Th2 Cell-Selective Enhancement of Human IL13 Transcription by IL13-1112C>T, a Polymorphism Associated with Allergic Inflammation

TL;DR: The findings suggest the nuclear milieu dictates the functional outcome of genetic variation in primary human and murine CD4+ Th2 lymphocytes and that increased expression of IL13-1112T in vivo may underlie its association with susceptibility to allergic inflammation.
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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