Department of Pulmonary Medicine, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima, Japan.
Front Immunol. 2022 Jul 13;13:930862. doi: 10.3389/fimmu.2022.930862. eCollection 2022.
T helper type 2 cells (Th2 cells) and group 2 innate lymphoid cells (ILC2s) play an important role in the pathophysiology of asthma, including airway eosinophilic inflammation. ILC2s are activated by epithelial-derived cytokines [interleukin-25 (IL-25), IL-33, and thymic stromal lymphopoietin (TSLP)] from airway epithelial cells, leading to the release of high amounts of type 2 cytokines, such as IL-5 and IL-13. ILC2s induce airway inflammation in an antigen-independent manner, and ILC2s are considered to be involved in the pathogenesis of asthma exacerbation. Furthermore, ILC2 activation might also confer steroid resistance. Many recent studies in humans and mice are increasingly demonstrating that the function of ILC2s is regulated not just by epithelial-derived cytokines but by a variety of cytokines and mediators derived from innate immune cells. Furthermore, the biologics targeting these cytokines and/or their receptors have been shown to reduce asthma exacerbations and improve lung function and quality of life in asthmatics. This article reviews the current treatment landscape for type 2 airway inflammation in asthma and discusses the therapeutic potential for targeting ILC2s.
辅助性 T 细胞 2 型（Th2 细胞）和 2 型固有淋巴细胞（ILC2）在哮喘的病理生理学中发挥着重要作用，包括气道嗜酸性粒细胞炎症。ILC2 被气道上皮细胞产生的上皮衍生细胞因子（白细胞介素 25 [IL-25]、IL-33 和胸腺基质淋巴细胞生成素 [TSLP]）激活，导致大量 2 型细胞因子（如 IL-5 和 IL-13）的释放。ILC2 以非抗原依赖的方式诱导气道炎症，并且 ILC2 被认为参与哮喘恶化的发病机制。此外，ILC2 的激活也可能导致类固醇耐药。越来越多的人类和小鼠的最近研究表明，ILC2 的功能不仅受到上皮衍生细胞因子的调节，还受到固有免疫细胞产生的各种细胞因子和介质的调节。此外，针对这些细胞因子及其受体的生物制剂已被证明可减少哮喘恶化并改善哮喘患者的肺功能和生活质量。本文综述了哮喘中 2 型气道炎症的当前治疗现状，并讨论了针对 ILC2 的治疗潜力。
