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      Interleukin-37b Suppressed ILC2s in Children with Allergic Rhinitis


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          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.


          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-18R α, and ICOSL was examined using RCR. The change of IL-37b protein level in serum during subcutaneous allergen immunotherapy (SCIT) was determined by ELISA.


          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-18R α, 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.


          Our findings highlight the role of IL-37b in the suppression of ILC2s and establish a new therapeutic target in AR.

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          Most cited references22

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          Nuocytes represent a new innate effector leukocyte that mediates type-2 immunity

          Innate immunity provides the first line of defence against invading pathogens and provides important cues for the development of adaptive immunity. Type-2 immunity – responsible for protective immune responses to helminth parasites1,2 and the underlying cause of the pathogenesis of allergic asthma3,4 – consists of responses dominated by the cardinal type-2 cytokines interleukin (IL)-4, IL-5 and IL-13 (ref. 5). T cells are an important source of these cytokines in adaptive immune responses, but the innate cell sources remain to be comprehensively elucidated. Here, through the use of novel Il13eGFP reporter mice, we present the identification and functional characterisation of a new innate type-2 immune effector leukocyte that we have named the nuocyte. Nuocytes expand in vivo in response to the type 2-inducing cytokines IL-25 and IL-33, and represent the predominant early source of IL-13 during helminth infection with Nippostrongylus brasiliensis. In the combined absence of IL-25 and IL-33 signalling, nuocytes fail to expand, resulting in a severe defect in worm expulsion that is rescued by the adoptive transfer of in vitro cultured wildtype, but not IL-13-deficient, nuocytes. Thus, nuocytes represent a critically important innate effector cell in type-2 immunity.
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            International Consensus Statement on Allergy and Rhinology: Allergic Rhinitis.

            Critical examination of the quality and validity of available allergic rhinitis (AR) literature is necessary to improve understanding and to appropriately translate this knowledge to clinical care of the AR patient. To evaluate the existing AR literature, international multidisciplinary experts with an interest in AR have produced the International Consensus statement on Allergy and Rhinology: Allergic Rhinitis (ICAR:AR).
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              Interleukin 37 is a fundamental inhibitor of innate immunity

              The function of interleukin 37 (formerly IL-1 family member 7) remains elusive. Expression of IL-37 in macrophages or epithelial cells imparted near complete suppression of pro-inflammatory cytokines, whereas the abundance of these cytokines increased with silencing of endogenous IL-37 in human blood cells. Anti-inflammatory cytokines remained unchanged under similar conditions. IL-37-transgenic mice were protected from lipopolysaccharide-induced shock, exhibiting markedly improved lung and kidney function and reduced liver damage. IL-37-transgenic mice had less circulating and tissue cytokines (72-95% lower) than wild-type mice and exhibited less dendritic cell activation. IL-37 interacted intracellularly with Smad3 and IL-37-expressing cells and transgenic mice exhibited less cytokine suppression when endogenous Smad3 was depleted. IL-37 thus emerges as a natural suppressor of innate inflammatory and immune responses.

                Author and article information

                Mediators Inflamm
                Mediators Inflamm
                Mediators of Inflammation
                14 April 2023
                : 2023
                : 1572891
                1Department of Otolaryngology, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangdong Provincial Clinical Research Center for Child Health, Guangzhou 510623, China
                2Department of Otolaryngology, Liuzhou hospital of Guangzhou Women and Children's Medical Center, Guangxi 545001, China
                3The Third People's Hospital of Dongguan, Dongguan Songshan Lake Center Hospital, Dongguan, China
                Author notes

                Academic Editor: Qingdong Guan

                Author information
                Copyright © 2023 Qingxiang Zeng et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                : 28 November 2022
                : 26 March 2023
                : 29 March 2023
                Funded by: National Natural Science Grant of China
                Award ID: 82271142
                Award ID: 81970861
                Funded by: Guangdong Province Natural Science Grant
                Award ID: 2021A1515010940
                Funded by: Guangzhou Science and Technology Program key projects
                Award ID: 202201011844
                Award ID: 202201020600
                Award ID: 202102020079
                Funded by: Dongguan Social Science and Technology Development (Key) Project
                Award ID: 20221800906162
                Funded by: Major Research and Cultivation Fund Project of Dongguan Songshan Lake Central Hospital
                Award ID: GZR002
                Research Article



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