Regulatory T cells are a double-edged sword in pulmonary fibrosis.

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.