Interleukin-37b Suppressed ILC2s in Children with Allergic Rhinitis

Author:

Zeng Qingxiang1ORCID,Zeng Yinhui1ORCID,Xiao Haiqing1,Li Jinyuan1,Yang Chao1,Luo Renzhong1ORCID,Liu Wenlong12ORCID,Wen Yanhui3ORCID

Affiliation:

1. Department of Otolaryngology, Guangzhou Women and Children’s Medical Center, Guangzhou Medical University, Guangdong Provincial Clinical Research Center for Child Health, Guangzhou 510623, China

2. Department of Otolaryngology, Liuzhou hospital of Guangzhou Women and Children’s Medical Center, Guangxi 545001, China

3. The Third People’s Hospital of Dongguan, Dongguan Songshan Lake Center Hospital, Dongguan, China

Abstract

Background. Interleukin-37b is a fundamental inhibitor of innate and acquired immunity. Type 2 innate lymphoid cells (ILC2s) can secret type 2 cytokines and regulate allergic rhinitis (AR). However, the role of IL-37b in ILC2s in children with AR was not clear. Methods. We recruited 15 AR children and controls. The serum IL-37b levels and its relation with the frequency and functional phenotype of ILC2s. The regulation of IL-37b on ILC2s proliferation and function was confirmed using flow cytometry and enzyme-linked immunosorbent assay (ELISA). The mRNA expression of IL-1R8, IL-18Rα, and ICOSL was examined using RCR. The change of IL-37b protein level in serum during subcutaneous allergen immunotherapy (SCIT) was determined by ELISA. Results. We have demonstrated that both of the frequencies of blood ILC2s, IL-5+ILC2s, and IL-13+ILC2s in AR children were elevated compared with controls. The serum protein level of IL-37b was downregulated in AR, and it was negatively related to the frequency of ILC2s, IL-5+ILC2s, and IL-13+ILC2s. IL-37b increased the mRNA levels of IL-1R8, IL-18Rα, and ICOSL expressed by ILC2s. IL-37b suppressed the proliferation of ILC2s and the secretion of IL-5 and IL-13 from ILC2s. Finally, we found that IL-37b was increased in AR children after 3 years’ SLIT, especially in the good response group. Conclusion. Our findings highlight the role of IL-37b in the suppression of ILC2s and establish a new therapeutic target in AR.

Funder

National Natural Science Grant of China

Publisher

Hindawi Limited

Subject

Cell Biology,Immunology

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