Department of Pathology, University of Michigan, Ann Arbor, MI, United States.
Mary H. Weiser Food Allergy Center, University of Michigan, Ann Arbor, MI, United States.
Front Immunol. 2021 Apr 19;12:675169. doi: 10.3389/fimmu.2021.675169. eCollection 2021.
Innate lymphoid type-2 cells (ILC2) are a population of innate cells of lymphoid origin that are known to drive strong Type 2 immunity. ILC2 play a key role in lung homeostasis, repair/remodeling of lung structures following injury, and initiation of inflammation as well as more complex roles during the immune response, including the transition from innate to adaptive immunity. Remarkably, dysregulation of this single population has been linked with chronic lung pathologies, including asthma, chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary fibrotic diseases (IPF). Furthermore, ILC2 have been shown to increase following early-life respiratory viral infections, such as respiratory syncytial virus (RSV) and rhinovirus (RV), that may lead to long-term alterations of the lung environment. The detrimental roles of increased ILC2 following these infections may include pathogenic chronic inflammation and/or alterations of the structural, repair, and even developmental processes of the lung. Respiratory viral infections in older adults and patients with established chronic pulmonary diseases often lead to exacerbated responses, likely due to previous exposures that leave the lung in a dysregulated functional and structural state. This review will focus on the role of ILC2 during respiratory viral exposures and their effects on the induction and regulation of lung pathogenesis. We aim to provide insight into ILC2-driven mechanisms that may enhance lung-associated diseases throughout life. Understanding these mechanisms will help identify better treatment options to limit not only viral infection severity but also protect against the development and/or exacerbation of other lung pathologies linked to severe respiratory viral infections.
固有淋巴样细胞 2 型（ILC2）是一类淋巴样来源的固有细胞，已知其能驱动强烈的 2 型免疫反应。ILC2 在肺稳态、损伤后肺结构的修复/重塑以及炎症的启动中发挥关键作用，在免疫反应中还发挥更复杂的作用，包括从先天免疫向适应性免疫的转变。值得注意的是，该单一群体的失调与慢性肺部疾病有关，包括哮喘、慢性阻塞性肺疾病（COPD）和特发性肺纤维化疾病（IPF）。此外，研究表明，在早期生命呼吸道病毒感染后，如呼吸道合胞病毒（RSV）和鼻病毒（RV），ILC2 会增加，这可能导致肺部环境的长期改变。这些感染后 ILC2 的增加可能会导致有害的作用，包括致病性慢性炎症和/或肺部结构、修复，甚至发育过程的改变。老年人和患有已确立的慢性肺部疾病的患者的呼吸道病毒感染常常导致加重的反应，这可能是由于先前的暴露使肺部处于失调的功能和结构状态。这篇综述将重点关注 ILC2 在呼吸道病毒暴露期间的作用及其对肺发病机制的诱导和调节的影响。我们旨在提供有关 ILC2 驱动机制的见解，这些机制可能会增强与生命全程相关的肺部疾病。了解这些机制将有助于确定更好的治疗选择，不仅限制病毒感染的严重程度，而且还可以预防与严重呼吸道病毒感染相关的其他肺部疾病的发展和/或加重。
