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The Cytokines of Asthma

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TLDR
The cytokine networks driving asthma are reviewed, placing these in cellular context and incorporating insights from cytokine-targeting therapies in the clinic, to argue that the development of new and improved therapeutics will require understanding the diverse mechanisms underlying the spectrum of asthma pathologies.
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This article is published in Immunity.The article was published on 2019-04-16 and is currently open access. It has received 501 citations till now. The article focuses on the topics: Bronchial hyperresponsiveness & Systemic inflammation.

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Citations
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Omalizumab is effective in allergic and non-allergic patients with nasal polyps and asthma

TL;DR: Omalizumab is a human anti-IgE mAb with proved efficacy in patients with severe allergic asthma as mentioned in this paper, which could be a treatment option for patients with nasal polyps and asthma.
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CCR5 attenuates neutrophilic airway inflammation exacerbated by infection with rhinovirus

TL;DR: The results suggest that CCR5 attenuates hRV-induced neutrophilic airway inflammation through conserving the equilibrium of CD4+Foxp3+ Treg cells and IL-17+CD4+ Th17 cells in hRv-induced asthma exacerbation, along with suppressing Th2 responses.

Aspergillus fumigatus–Secreted Alkaline Protease 1 Mediates Airways Hyperresponsiveness in Severe Asthma

TL;DR: It is demonstrated that the serine protease Alp1 from the ubiquitous mold and allergen, Aspergillus fumigatus, can induce AHR in mice unable to generate eosinophilic inflammation and point to a new target for direct intervention of fungal-associated asthma.
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Dexmedetomidine alleviates airway hyperresponsiveness and allergic airway inflammation through the TLR4/NF-κB signaling pathway in mice

TL;DR: In the murine OVA-induced asthma model, DEX decreased AHR following Mch inhalation and reduced the infiltration of inflammatory cells, and it is suggested that DEX may represent a potential anti-inflammatory agent for the treatment and management of patients with asthma.
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A pathogenic integrated view explaining the different endotypes of asthma and allergic disorders

TL;DR: This review proposes some immunopathogenic scenarios characterizing the principal endotypes which can be associated with a precise phenotype of asthma, and indicates that similar concepts can also be applied to the inflammation of other non‐respiratory allergic disorders.
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.
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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.
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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.
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.
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Trending Questions (1)
What is the role of cytokines in the pathogenesis of asthma?

The role of cytokines in the pathogenesis of asthma is to promote airway eosinophilia, mucus overproduction, bronchial hyperresponsiveness, and immunoglobulin E synthesis.