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

IF 4.4 3区 医学 Q2 CELL BIOLOGY Mediators of Inflammation Pub Date : 2024-11-06 eCollection Date: 2024-01-01 DOI:10.1155/2024/9692031
Xiaowei Qin, Chunrui Wang, Jueqi Li, Xiaopeng Zhang, Tianhong Zhang
{"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。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
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.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
Mediators of Inflammation
Mediators of Inflammation 医学-免疫学
CiteScore
8.70
自引率
0.00%
发文量
202
审稿时长
4 months
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.
期刊最新文献
Sublingual Immunotherapy Decreased the Serum Levels of Interleukin-36γ in Allergic Rhinitis. The Role of Ca2+/PI3K/Akt/eNOS/NO Pathway in Astragaloside IV-Induced Inhibition of Endothelial Inflammation Triggered by Angiotensin II. ITGA1 Promotes Glioma Cell Proliferation and Affects Immune Cell Infiltration in Low-Grade Glioma. The AMPK-mTOR Pathway Is Inhibited by Chaihu Shugan Powder, Which Relieves Nonalcoholic Steatohepatitis by Suppressing Autophagic Ferroptosis. Functional Involvement of TANK-Binding Kinase 1 in the MyD88-Dependent NF-κB Pathway Through Syk.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1