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Journal ArticleDOI

The immunology of asthma

Bart N. Lambrecht, +1 more
- 01 Jan 2015 - 
- Vol. 16, Iss: 1, pp 45-56
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TLDR
Results from in-depth molecular studies of mouse models in light of the results from the first clinical trials targeting key cytokines in humans are discussed and the extraordinary heterogeneity of asthma is described.
Abstract
Asthma is a common disease that affects 300 million people worldwide. Given the large number of eosinophils in the airways of people with mild asthma, and verified by data from murine models, asthma was long considered the hallmark T helper type 2 (T(H)2) disease of the airways. It is now known that some asthmatic inflammation is neutrophilic, controlled by the T(H)17 subset of helper T cells, and that some eosinophilic inflammation is controlled by type 2 innate lymphoid cells (ILC2 cells) acting together with basophils. Here we discuss results from in-depth molecular studies of mouse models in light of the results from the first clinical trials targeting key cytokines in humans and describe the extraordinary heterogeneity of asthma.

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Citations
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Th9 and other IL-9-producing cells in allergic asthma.

TL;DR: The role of Th9 and IL-9-producing cells in allergic asthma is reviewed, which has been demonstrated to be involved in several diseases, such as cancer, autoimmunity and other pathogen-mediated immune-regulated diseases.
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Airway microbial dysbiosis in asthmatic patients: A target for prevention and treatment?

TL;DR: A better understanding of the regulation of both the lung and gut microbiota to derive appropriate targets for prevention or treatment of asthma is needed.
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The microbiome in asthma.

TL;DR: This review summarizes the most recent findings on how asthma development is connected with respiratory and intestinal microbial dysbiosis and highlights and discusses recent research that reveals the existence of a ‘gut–lung’ microbial axis and its impact on asthma development.
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Apoptotic Cell Clearance by Bronchial Epithelial Cells Critically Influences Airway Inflammation

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Regulation of type 2 innate lymphoid cell-dependent airway hyperreactivity by butyrate.

TL;DR: The findings identify butyrate as a critical regulator of ILC2 proliferation and function through its HDAC inhibitory activity and can serve as a potential therapeutic target for asthma.
References
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Journal ArticleDOI

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

Interleukin-13: Central Mediator of Allergic Asthma

TL;DR: In this paper, 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.
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 Article

Interleukin-13: Central mediator of allergic asthma

TL;DR: 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.
Journal ArticleDOI

Asthma phenotypes: the evolution from clinical to molecular approaches

TL;DR: Ongoing studies of large-scale, molecularly and genetically focused and extensively clinically characterized cohorts of asthma should enhance the ability to molecularly understand these phenotypes and lead to more targeted and personalized approaches to asthma therapy.
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