Abstract
Editorial summaryAirway inflammation is key to the severity and persistence of asthma. Recent studies have revealed novel immune mechanisms that target dendritic cells, T helper 2 cytokines, regulatory T cells, and type 2 innate lymphoid cells in allergic inflammation, as well as novel approaches that target airway smooth muscle in asthma. These advances inform the development of new targeted treatments for allergic inflammation and asthma with the potential to provide therapeutic benefit.
Highlights
Airway inflammation is key to the severity and persistence of asthma
In mild-to-moderate asthma, the predominant inflammatory response in the airway is T helper 2 (Th2)-type inflammation ( known as type 2 (T2) inflammation), which is driven by CD4+ helper T cells that express the cytokines IL-13, IL-4, and IL-5 and is associated with elevated levels of immunoglobulin E (IgE) and eosinophils in the airways
Monoclonal antibodies have been developed to another type 2 cytokine, thymic stromal lymphopoietin (TSLP), which was implicated in asthma using genomewide association studies (GWAS), and these TSLP monoclonal antibodies were recently tested in a clinical trial [6]
Summary
Airway inflammation is key to the severity and persistence of asthma. Recent studies have revealed novel immune mechanisms that target dendritic cells, T helper 2 cytokines, regulatory T cells, and type 2 innate lymphoid cells in allergic inflammation, as well as novel approaches that target airway smooth muscle in asthma. T2 inflammation is present in all three types of asthma (mild, moderate, and severe). There has been a proliferation of studies that have revealed the mechanisms underlying allergic inflammation and asthma, and are providing possible novel approaches for treatment.
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