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Open AccessJournal ArticleDOI

Th17-mediated inflammation in asthma

TLDR
The role of Th17 cells in asthma will be answered in ongoing clinical trials with therapeutics targeting IL- 17A and IL-17 receptor signaling.
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This article is published in Current Opinion in Immunology.The article was published on 2013-12-01 and is currently open access. It has received 247 citations till now. The article focuses on the topics: Proinflammatory cytokine & Inflammation.

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Citations
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Mechanisms Driving Gender Differences in Asthma

TL;DR: Overall, ovarian hormones increased and testosterone decreased airway inflammation in asthma, but the mechanisms remain unclear, which will help determine if women with asthma should take (or avoid) hormonal contraceptives as well as predict changes in asthma symptoms during life phases, including pregnancy and menopause.
Journal ArticleDOI

The cell biology of asthma

TL;DR: The clinical manifestations of asthma are caused by obstruction of the conducting airways of the lung as mentioned in this paper, and two airway cell types are critical for asthma pathogenesis: epithelial cells and smooth muscle cells.
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Cellular mechanisms underlying eosinophilic and neutrophilic airway inflammation in asthma.

TL;DR: The recent advances in the knowledge of the cellular and molecular mechanisms underlying asthmatic inflammation are contributing to the identification of novel therapeutic targets, potentially suitable for the implementation of future improvements in antiasthma pharmacologic treatments.
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Chitinase-like proteins promote IL-17-mediated neutrophilia in a tradeoff between nematode killing and host damage

TL;DR: It is found that Ym1 and Ym2 induced the accumulation of neutrophils through the expansion of γδ T cell populations that produced interleukin 17 (IL-17), which suggested that regulation of IL-17 is an inherent feature of mouse CLPs.
References
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Interleukin 17–producing CD4 + effector T cells develop via a lineage distinct from the T helper type 1 and 2 lineages

TL;DR: Findings provide a basis for understanding how inhibition of IFN-γ signaling enhances development of pathogenic TH-17 effector cells that can exacerbate autoimmunity.
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IL-17 and Th17 Cells.

TL;DR: The investigation of the differentiation, effector function, and regulation of Th17 cells has opened up a new framework for understanding T cell differentiation and now appreciate the importance of Th 17 cells in clearing pathogens during host defense reactions and in inducing tissue inflammation in autoimmune disease.
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Lebrikizumab Treatment in Adults with Asthma

TL;DR: Lebrikizumab treatment was associated with improved lung function and patients with high pretreatment levels of serum periostin had greater improvement in lung function with lebrikIZumab than did patients with low periOSTin levels.
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Interleukin-17 and type 17 helper T cells.

TL;DR: Type 17 helper T cells (Th17) — a third class of T cells — and their major cytokine, interleukin-17, are essential for the defense against certain fungi, extracellular bacteria, and Mycob bacteria.
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IL-22 mediates mucosal host defense against Gram-negative bacterial pneumonia

TL;DR: Although both cytokines regulated CXC chemokines and granulocyte colony–stimulating factor production in the lung, only IL-22 increased lung epithelial cell proliferation and increased transepithelial resistance to injury, and data support the concept that the TH17 cell lineage and its effector molecules have evolved to effect host defense against extracellular pathogens at mucosal sites.
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