Department of Anesthesiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China; Institute of Anesthesia and Critical Care Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.
Department of Anesthesiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China; Institute of Anesthesia and Critical Care Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.
Int Immunopharmacol. 2020 Jul;84:106443. doi: 10.1016/j.intimp.2020.106443. Epub 2020 Apr 22.
Pulmonary fibrosis (PF) is a chronic progressive interstitial lung disease. The pathogenesis of PF has not been clearly elucidated, and there is no obvious effective treatment to arrest the progression of PF to date. A long-term chronic inflammatory response and inappropriate repair process after lung injury are important causes and pathological processes of PF. As an influential type of the body's immune cells, regulatory T cells (Tregs) play an irreplaceable role in inhibiting the inflammatory response and promoting the repair of lung tissue. However, the exact roles of Tregs in the process of PF have not been clearly established, and the available literature concerning the roles of Tregs in PF are contradictory. First, Tregs can advance the progression of pulmonary fibrosis by secreting platelet-derived growth factor (PDGF), transforming growth factor-β (TGF-β) and other related factors, promoting epithelial-mesenchymal transition (EMT) and affecting the Th1 and Th2 balance, etc. Second, Tregs can inhibit PF by promoting the repair of epithelial cell damage, inhibiting the accumulation of fibroblasts, and strongly inhibiting the production and function of other related pro-inflammatory factors and pro-inflammatory cells. Accordingly, in this review, we focus on the multiple roles of Tregs in different models and different pulmonary fibrosis phases, thereby providing theoretical support for a better understanding of the multiple roles of these cells in PF and a theoretical basis for identifying targets for PF therapy.
肺纤维化（PF）是一种慢性进行性间质性肺疾病。PF 的发病机制尚未阐明，迄今为止，没有明显有效的治疗方法可以阻止 PF 的进展。肺损伤后的长期慢性炎症反应和不当修复过程是 PF 的重要原因和病理过程。调节性 T 细胞（Tregs）作为机体免疫细胞的一种有影响力的类型，在抑制炎症反应和促进肺组织修复方面发挥着不可替代的作用。然而，Tregs 在 PF 过程中的确切作用尚未明确确定，并且关于 Tregs 在 PF 中的作用的现有文献存在矛盾。首先，Tregs 可以通过分泌血小板衍生生长因子（PDGF）、转化生长因子-β（TGF-β）和其他相关因子，促进上皮间质转化（EMT）和影响 Th1 和 Th2 平衡等，促进肺纤维化的进展。其次，Tregs 可以通过促进上皮细胞损伤的修复、抑制成纤维细胞的积累以及强烈抑制其他相关促炎因子和促炎细胞的产生和功能，来抑制 PF。因此，在这篇综述中，我们重点关注 Tregs 在不同模型和不同肺纤维化阶段的多种作用，从而为更好地理解这些细胞在 PF 中的多种作用提供理论支持，并为确定 PF 治疗靶点提供理论依据。
