Group 2 innate lymphoid cells (ILC2s) are important in typical type 2 immune-mediated diseases and an essential therapeutic target

The prevalence rate of allergic diseases, such as asthma, atopic rhinitis (AR), and atopic dermatitis (AD), has been significantly increasing over the years because of environmental changes. Type 2 immunity is mediated by allergic inflammation initiated by an innate immune response. This response is...

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Bibliographic Details
Published in:Journal of International Medical Research 2022-01, Vol.50 (1), p.3000605211053156-3000605211053156
Main Authors: Jin, Jie, Sunusi, Sadik, Lu, Hongyan
Format: Article
Language:English
Subjects:
Asthma
Asthma - drug therapy
Cytokines
Eczema
Humans
Immunity, Innate
Inflammation
Lymphocytes
Review
Rhinitis, Allergic
Th2 Cells
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Summary:The prevalence rate of allergic diseases, such as asthma, atopic rhinitis (AR), and atopic dermatitis (AD), has been significantly increasing over the years because of environmental changes. Type 2 immunity is mediated by allergic inflammation initiated by an innate immune response. This response is orchestrated by type 2 cytokines (interleukin [IL]-4, IL-5, IL-9, and IL-13) together with other cells. The dendritic cell [DC]-T helper 2 (Th2) cell axis is the conventional type 2 immune pathway, and is currently known as the group 2 innate lymphoid cell (ILC2)-DC-Th2 axis that mediates type 2 inflammation. ILC2s strongly mediate type 2 inflammation in allergic diseases. ILC2s are activated by epithelial cell-derived cytokines, such as IL-25 and IL-33, and thymic stromal lymphopoietin. Additionally, ILC2s are activated by mast cell lipid inflammatory mediators, such as cysteinyl leukotrienes and prostaglandin D2. ILC2s produce a large amount of type 2 cytokines. The important role of ILC2s in the pathogenesis of type 2-mediated disease has resulted in ILC2-derived cytokines being a target for therapeutic development. In this review, we discuss type 2 immunity, mainly the ILC2-DC-Th2 axis, and other immune cells, the dominant role of ILC2s in asthma, AR, and AD, and therapeutic targets against type 2 cytokines.
ISSN:0300-0605
1473-2300
DOI:10.1177/03000605211053156