上皮源性细胞因子IL-33、IL-25和TSLP在哮喘发病机制中的作用  

Roles of epithelial-derived cytokines IL-33,IL-25 and TSLP in the pathogenesis of asthma

作　　者：张鑫[1] 王炜[1] 孙英[1] ZHANG Xin WANG Wei SUN Ying(Department of Immunology, School of Basic Medical Sciences, Capital Medical University, Beijing 100069, China)

机构地区：[1]首都医科大学基础医学院免疫学系,北京100069

出　　处：《微生物学免疫学进展》2017年第5期53-58,共6页Progress In Microbiology and Immunology

基　　金：国家自然科学基金(81373177;81471594)

摘　　要：哮喘(asthma)是一种以气道高反应性、慢性气道炎症、气道重塑和可逆性的气流受阻为特征的常见慢性呼吸系统疾病。近年来,研究发现气道上皮细胞在霉菌、尘螨、花粉、病毒感染、空气污染物等各种损伤因素的作用下,可释放细胞因子白细胞介素-33(interleukin-33,IL-33)、白细胞介素-25(interleukin-25,IL-25)和胸腺基质淋巴细胞生成素(thymic stromal lymphopoietin,TSLP),这些细胞因子不仅可作用于2型辅助性T细胞(type 2 helper T cells,Th2 cells),同时也可作用于固有淋巴样2型细胞(group 2 innate lymphoid cells,ILC2s),通过释放Th2型细胞因子,参与哮喘的发生与发展。尽管这3种细胞因子在哮喘的发生与发展中均起到重要作用,但其在哮喘病理、生理学效应及作用方式上并非完全相同。现就这3种上皮源性细胞因子IL-33、IL-25和TSLP在哮喘发病机制中的作用作一概述。Asthma is a common chronic respiratory disease characterized by hyper-responsiveness,chronic inflammation,remodeling in airways and reversible airflows obstruction. Recent studies have shown that airway epithelial cells can release cytokines interleukin-33（ IL-33）,interleukin-25（ IL-25） and thymic stromal lymphopoietin（ TSLP） under the action of various damage factors such as molds,dust mites and its metabolites,pollens,virus infections and air pollutants. The three epithelial-derived cytokines can not only act on type 2 helper T cells,but also stimulate group 2 innate lymphoid cells leading to release Th2 type cytokines,involved in the development of asthma. Although they play an important role in the occurrence and development of asthma,but the three cytokines are not exactly same in the efficacy of pathophysiology and action modes. This review briefly summarizes the roles of IL-33,IL-25 and TSLP in the pathogenesis of asthma.

关 键 词：哮喘 白细胞介素-33 白细胞介素-25 胸腺基质淋巴细胞生成素 

分 类 号：R562.25[医药卫生—呼吸系统]