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白细胞介素-32:在哮喘中的作用及其作为治疗剂的潜力。

Interleukin-32: its role in asthma and potential as a therapeutic agent.

机构信息

Department of Respiratory Medicine, the Second Hospital of Jilin University, Changchun, Jilin, China.

Department of Gastrointestinal medicine, the Second Hospital of Jilin University, Changchun, Jilin, China.

出版信息

Respir Res. 2018 Jun 25;19(1):124. doi: 10.1186/s12931-018-0832-x.

DOI:10.1186/s12931-018-0832-x
PMID:29940981
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6019726/
Abstract

Interleukin (IL)-32, also named natural killer cell transcript 4 (NK4), has increasingly been described as an immunoregulator that controls cell differentiation and cell death and is involved in the stimulation of anti-/pro-inflammatory cytokines. Abnormal presence of IL-32 has been repeatedly noticed during the pathogenesis of allergic, infectious, cancerous, and inflammatory diseases. Of particular note was the observation of the anti-inflammatory property of IL-32 in a murine ovalbumin model of allergic asthma. Compared to wild-type mice, IL-32γ transgenic mice show decreased levels of inflammatory cells, recruited eosinophils, and lymphocytes in bronchoalveolar lavage fluid in a mouse model of acute asthma. To date, the molecular mechanism underlying the role of IL-32 in asthma remains to be elucidated. This review aims to summarize recent advances in the pathophysiology of asthma and describe the links to IL-32. The possibilities of using IL-32 as an airway inflammation biomarker and an asthma therapeutic agent are also evaluated.

摘要

白细胞介素 (IL)-32,也称为自然杀伤细胞转录因子 4 (NK4),越来越多地被描述为一种免疫调节剂,可控制细胞分化和细胞死亡,并参与刺激抗/促炎细胞因子。在过敏、感染、癌症和炎症性疾病的发病机制中,反复注意到 IL-32 的异常存在。特别值得注意的是,在变应原性哮喘的小鼠卵清蛋白模型中观察到 IL-32 的抗炎特性。与野生型小鼠相比,IL-32γ 转基因小鼠在急性哮喘小鼠模型中支气管肺泡灌洗液中的炎症细胞、募集的嗜酸性粒细胞和淋巴细胞水平降低。迄今为止,IL-32 在哮喘中的作用的分子机制仍有待阐明。本综述旨在总结哮喘病理生理学的最新进展,并描述与 IL-32 的联系。还评估了将 IL-32 用作气道炎症生物标志物和哮喘治疗剂的可能性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55ad/6019726/6224ae018b26/12931_2018_832_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55ad/6019726/ad641be237ca/12931_2018_832_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55ad/6019726/6224ae018b26/12931_2018_832_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55ad/6019726/ad641be237ca/12931_2018_832_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55ad/6019726/6224ae018b26/12931_2018_832_Fig2_HTML.jpg

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Front Immunol. 2024 Aug 15;15:1437224. doi: 10.3389/fimmu.2024.1437224. eCollection 2024.
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