{"title":"Sublingual Immunotherapy Decreased the Serum Levels of Interleukin-36<i>γ</i> in Allergic Rhinitis.","authors":"Xiaowei Qin, Chunrui Wang, Jueqi Li, Xiaopeng Zhang, Tianhong Zhang","doi":"10.1155/2024/9692031","DOIUrl":null,"url":null,"abstract":"<p><p><b>Background:</b> Allergy immunotherapy (AIT), a treatment approach for allergic rhinitis (AR), is recognized for its potential to modify the disease course beyond mere symptom relief. Interleukin-36<i>γ</i> (IL-36<i>γ</i>), a key player in immune responses, has been implicated in promoting eosinophilic inflammation in AR by activating eosinophils. We aimed to investigate the effect of IL-36<i>γ</i> on group II lymphoid cell (ILC2) in AR patients who underwent sublingual immunotherapy (SLIT). <b>Methods:</b> Twenty-four AR patients were enrolled and administered with SLIT. Serum proteins of IL-36<i>γ</i>, interleukin-5 (IL-5), and interleukin-13 (IL-13) during SLIT were quantitatively assessed using enzyme-linked immunosorbent assay (ELISA). The proportion of ILC2 was determined by flow cytometry. Sorted ILC2s were stimulated by IL-36<i>γ</i> and ILC2 cell differentiation, and type II cytokines expression were examined. <b>Results:</b> SLIT treatment decreased the serum protein levels of IL-36<i>γ</i>, IL-5, IL-13, and the proportion of ILC2 significantly. IL-36<i>γ</i> suppressed the proliferation of ILC2 by inhibiting the levels of ILC2 transcription factor. IL-36<i>γ</i> also inhibited IL-5 and IL-13 expression from ILC2. <b>Conclusion:</b> The changes of IL-36<i>γ</i> during SLIT were related to the inhibited function of ILC2, implying that IL-36<i>γ</i> may be used as a new biomarker for monitoring the efficacy of SLIT in AR.</p>","PeriodicalId":18371,"journal":{"name":"Mediators of Inflammation","volume":"2024 ","pages":"9692031"},"PeriodicalIF":4.4000,"publicationDate":"2024-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11561173/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Mediators of Inflammation","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1155/2024/9692031","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/1/1 0:00:00","PubModel":"eCollection","JCR":"Q2","JCRName":"CELL BIOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Background: Allergy immunotherapy (AIT), a treatment approach for allergic rhinitis (AR), is recognized for its potential to modify the disease course beyond mere symptom relief. Interleukin-36γ (IL-36γ), a key player in immune responses, has been implicated in promoting eosinophilic inflammation in AR by activating eosinophils. We aimed to investigate the effect of IL-36γ on group II lymphoid cell (ILC2) in AR patients who underwent sublingual immunotherapy (SLIT). Methods: Twenty-four AR patients were enrolled and administered with SLIT. Serum proteins of IL-36γ, interleukin-5 (IL-5), and interleukin-13 (IL-13) during SLIT were quantitatively assessed using enzyme-linked immunosorbent assay (ELISA). The proportion of ILC2 was determined by flow cytometry. Sorted ILC2s were stimulated by IL-36γ and ILC2 cell differentiation, and type II cytokines expression were examined. Results: SLIT treatment decreased the serum protein levels of IL-36γ, IL-5, IL-13, and the proportion of ILC2 significantly. IL-36γ suppressed the proliferation of ILC2 by inhibiting the levels of ILC2 transcription factor. IL-36γ also inhibited IL-5 and IL-13 expression from ILC2. Conclusion: The changes of IL-36γ during SLIT were related to the inhibited function of ILC2, implying that IL-36γ may be used as a new biomarker for monitoring the efficacy of SLIT in AR.
期刊介绍:
Mediators of Inflammation is a peer-reviewed, Open Access journal that publishes original research and review articles on all types of inflammatory mediators, including cytokines, histamine, bradykinin, prostaglandins, leukotrienes, PAF, biological response modifiers and the family of cell adhesion-promoting molecules.