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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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Does the epithelial barrier hypothesis explain the increase in allergy, autoimmunity and other chronic conditions?

TL;DR: Akdis et al. as discussed by the authors introduced an extended "epithelial barrier hypothesis" which proposes that the increase in epithelial barrier-damaging agents linked to industrialization, urbanization and modern life underlies the rise in allergic, autoimmune and other chronic conditions.
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The basic immunology of asthma

TL;DR: In this article, the underlying immunological basis of various asthma endotypes by discussing results obtained from animal studies as well as results generated in clinical studies targeting specific immune pathways is discussed.
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The cytokine network involved in the host immune response to periodontitis

TL;DR: This review begins with an up-to-date aetiological hypothesis of periodontal disease and summarize the roles of cytokines in the host immune response and the latest cytokine-related therapeutic measures for periodontic disease.
References
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Pulmonary neuroendocrine cells amplify allergic asthma responses

TL;DR: In vitro data show that pulmonary neuroendocrine cells (PNECs), a rare airway epithelial cell population, can act as chemosensors, and the underlying mechanisms by identifying molecular effectors and cellular targets of PNECs are elucidated.
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Environmental allergens induce allergic inflammation through proteolytic maturation of IL-33

TL;DR: A broad range of allergens across multiple kingdoms can directly cleave IL-33 via their intrinsic protease activity and convert it into a highly active processed form and reveal a molecular mechanism for the rapid induction of allergic type 2 inflammation following allergen exposure.
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Increased frequency of dual-positive TH2/TH17 cells in bronchoalveolar lavage fluid characterizes a population of patients with severe asthma.

TL;DR: Asthma is associated with a higher frequency of dual-positive TH2/TH17 cells in BAL fluid, and the TH2-predominant subgroup manifested the most severe form of asthma, whereas the TH-2-TH17(low) subgroup had the mildest asthma.
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Interleukin-2-Dependent Allergen-Specific Tissue-Resident Memory Cells Drive Asthma

TL;DR: Investigation into the differentiation of pathogenic Trm cells revealed that interleukin-2 (IL-2) signaling was required for residency and directed a program of tissue homing migrational cues that identified IL-2-dependent resident Th2 memory cells as drivers of lung allergic responses.
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Chitin activates parallel immune modules that direct distinct inflammatory responses via innate lymphoid type 2 and γδ T cells.

TL;DR: Inhaled chitin elicited patterns of innate cytokines that targeted distinct populations of resident lymphoid cells, revealing divergent but interacting pathways underlying the tissue accumulation of specific types of inflammatory myeloid cells.
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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.