The role of group 2 innate lymphoid cells (ILC2) in respiratory allergic diseases: An update.
- Author:
Chao LUO
1
;
Shaobo LIU
1
;
Quanwei REN
1
;
Shunlin PENG
2
Author Information
1. Department of Otolaryngology, Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu 610075, China.
2. Department of Otolaryngology, Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu 610075, China. *Corresponding author, E-mail: psl6@163.com.
- Publication Type:Journal Article
- MeSH:
Humans;
Immunity, Innate;
Interleukin-4;
Interleukin-9;
Lymphocytes;
Hypersensitivity;
Cytokines;
Respiratory Tract Diseases;
Inflammation
- From:
Chinese Journal of Cellular and Molecular Immunology
2023;39(6):552-557
- CountryChina
- Language:Chinese
-
Abstract:
Group 2 innate lymphoid cells (ILC2s) are the "mirror cells" of Th2 cells. Although the total cell number of ILC2s is far less than that of CD4+ Th2 cells in the body, the activated ILC2s have a more powerful biological activity than CD4+ Th2 cells and can rapidly enhanced Th2-cell inflammatory reaction. It plays an important role in the pathogenesis of allergic respiratory diseases. The transmitters that activate ILC2s include inflammatory cytokines (IL-33, IL-25, TSLP, IL-4, IL-9), lipid transmitters (prostaglandins, leukotrienes), and other activating transmitters (ICOS, Complement C3a, neuropeptide receptor, vasoactive intestinal peptide and calcitonin gene-related peptide, etc). Activated ILC2s produce large amounts of IL-4, IL-5, IL-9, IL-13, and amphiregulin and other inflammatory mediators, and induce airway hyperresponsiveness, mucus secretion and airway remodeling and other respiratory allergic reactions. Therefore, respiratory allergic diseases, especially steroid-dependent asthma, could be treated potentially by inhibiting the activation of ILC2s. Hereby, we summarized the immunobiology of ILC2s, the initiation of ILC2s in allergic inflammation, the relationship between ILC2s and respiratory allergic diseases, and the recent advances in biological agents targeted by ILC2s.
