{"title":"舌下免疫疗法可降低过敏性鼻炎患者血清中的白细胞介素-36γ水平","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":"{\"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}","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
摘要
背景:过敏免疫疗法(AIT)是一种治疗过敏性鼻炎(AR)的方法,其改变病程的潜力已得到公认,而不仅仅是缓解症状。白细胞介素-36γ(IL-36γ)是免疫反应中的一个关键因子,被认为通过激活嗜酸性粒细胞促进了 AR 中的嗜酸性粒细胞炎症。我们旨在研究 IL-36γ 对接受舌下免疫疗法(SLIT)的 AR 患者中 II 组淋巴细胞(ILC2)的影响。研究方法24名AR患者接受了舌下免疫疗法(SLIT)。使用酶联免疫吸附试验(ELISA)定量评估 SLIT 期间血清中的 IL-36γ、白细胞介素-5(IL-5)和白细胞介素-13(IL-13)蛋白。流式细胞术测定了 ILC2 的比例。用 IL-36γ 刺激分选的 ILC2,检测 ILC2 细胞分化和 II 型细胞因子的表达。结果SLIT治疗显著降低了血清中IL-36γ、IL-5、IL-13的蛋白水平和ILC2的比例。IL-36γ通过抑制ILC2转录因子的水平来抑制ILC2的增殖。IL-36γ 还能抑制 ILC2 中 IL-5 和 IL-13 的表达。结论SLIT期间IL-36γ的变化与ILC2的功能受抑制有关,这意味着IL-36γ可作为一种新的生物标志物用于监测SLIT对AR的疗效。
Sublingual Immunotherapy Decreased the Serum Levels of Interleukin-36γ in Allergic Rhinitis.
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.