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Year : 2018  |  Volume : 131  |  Issue : 16  |  Page : 1983-1989

Potential Role of Interleukin-25/Interleukin-33/Thymic Stromal Lymphopoietin-Fibrocyte Axis in the Pathogenesis of Allergic Airway Diseases

1 Department of Respiratory Medicine, Beijing Tongren Hospital, Capital Medical University, Beijing 100730, China
2 Department of Otolaryngology Head and Neck Surgery, Beijing Tongren Hospital, Capital Medical University, Beijing 100730, China

Correspondence Address:
Dr. Xiao-Fang Liu
Department of Respiratory Medicine, Beijing Tongren Hospital, Capital Medical University, Beijing 100730
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0366-6999.238150

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Objective: Allergic airway diseases (AADs) are a group of heterogeneous disease mediated by T-helper type 2 (Th2) immune response and characterized with airway inflammation and remodeling, including allergic asthma, allergic rhinitis, and chronic rhinosinusitis with allergic background. This review aimed to discuss the abnormal epithelial-mesenchymal crosstalk in the pathogenesis of AADs. Data Sources: Articles referred in this review were collected from the database of PubMed published in English up to January 2018. Study Selection: We had done a literature search using the following terms “allergic airway disease OR asthma OR allergic rhinitis OR chronic sinusitis AND IL-25 OR IL-33 OR thymic stromal lymphopoietin OR fibrocyte”. Related original or review articles were included and carefully analyzed. Results: It is now believed that abnormal epithelial-mesenchymal crosstalk underlies the pathogenesis of AADs. However, the key regulatory factors and molecular events involved in this process still remain unclear. Epithelium-derived triple cytokines, including interleukin (IL)-25, IL-33, and thymic stromal lymphopoietin (TSLP), are shown to act on various target cells and promote the Th2 immune response. Circulating fibrocyte is an important mesenchymal cell that can mediate tissue remodeling. We previously found that IL-25-circulating fibrocyte axis was significantly upregulated in patients with asthma, which may greatly contribute to asthmatic airway inflammation and remodeling. Conclusions: In view of the redundancy of cytokines and “united airway” theory, we propose a new concept that IL-25/IL-33/TSLP-fibrocyte axis may play a vital role in the abnormal epithelial-mesenchymal crosstalk in some endotypes of AADs. This novel idea will guide potential new intervention schema for the common treatment of AADs sharing common pathogenesis in the future.


 Abstract in Chinese



目的:过敏性气道疾病(Allergic airway diseases , AADs)是一组Th2型免疫反应介导的慢性气道炎症和异常修复的异质性疾病群,包括具有过敏背景的某些过敏性哮喘、过敏性鼻炎和慢性鼻窦炎亚型。本综述旨在探讨上皮-间质异常通讯在过敏性气道疾病发病机制中的作用。


资料选择:我们用“(allergic airway disease OR asthma OR allergic rhinitis OR chronic sinusitis) AND (IL-25 OR IL-33 OR thymic stromal lymphopoietin OR fibrocyte)”这一检索式进行文献检索,并仔细阅读和分析相关研究论文或综述。

结果:目前认为上皮-间质异常通讯是过敏性气道疾病的核心发病机制,但参与其中的关键调控因子和分子事件尚未明确。IL-25/IL-33/TSLP(胸腺基质淋巴生成素)是上皮来源的促Th2型免疫反应的细胞因子,而循环纤维细胞(circulating fibrocyte)是一种可介导组织重塑的重要间质细胞。我们前期研究发现IL-25-fibrocyte轴在哮喘患者中表达明显上调,且和哮喘严重程度相关。


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