Division of Pulmonary and Critical Care Medicine, Department of Medicine.
Simpson Querrey Lung Institute for Translational Science.
J Clin Invest. 2023 Jul 17;133(14):e170505. doi: 10.1172/JCI170505.
Acute respiratory infections trigger an inflammatory immune response with the goal of pathogen clearance; however, overexuberant inflammation causes tissue damage and impairs pulmonary function. CD4+FOXP3+ regulatory T cells (Tregs) interact with cells of both the innate and the adaptive immune system to limit acute pulmonary inflammation and promote its resolution. Tregs also provide tissue protection and coordinate lung tissue repair, facilitating a return to homeostatic pulmonary function. Here, we review Treg-mediated modulation of the host response to respiratory pathogens, focusing on mechanisms underlying how Tregs promote resolution of inflammation and repair of acute lung injury. We also discuss potential strategies to harness and optimize Tregs as a cellular therapy for patients with severe acute respiratory infection and discuss open questions in the field.
急性呼吸道感染会引发炎症免疫反应，其目的是清除病原体；然而，过度的炎症会导致组织损伤并损害肺功能。CD4+FOXP3+调节性 T 细胞（Tregs）与先天和适应性免疫系统的细胞相互作用，以限制急性肺炎症并促进其消退。Tregs 还提供组织保护并协调肺组织修复，促进肺功能恢复到稳定状态。在这里，我们综述了 Treg 介导的宿主对呼吸道病原体反应的调节，重点介绍了 Tregs 促进炎症消退和急性肺损伤修复的机制。我们还讨论了利用和优化 Tregs 作为严重急性呼吸道感染患者细胞治疗的潜在策略，并讨论了该领域的悬而未决的问题。
