Imbalance of dendritic cell function in pulmonary fibrosis

Pulmonary fibrosis (PF) is a chronic, irreversible interstitial lung disease. The pathogenesis of PF remains unclear, and there are currently no effective treatments or drugs that can completely cure PF. The primary cause of PF is an imbalance of inflammatory response and inappropriate repair following lung injury. Dendritic cells (DCs), as one of the immune cells in the body, play an important role in regulating immune response, immune tolerance, and promoting tissue repair following lung injury. However, the role of DCs in the PF process is ambiguous or even contradictory in the existing literature. On the one hand, DCs can secrete transforming growth factor β(TGF-β), stimulate Th17 cell differentiation, stimulate fibroblast proliferation, and promote the generation of inflammatory factors interleukin-6(IL-6) and tumor necrosis factor-α(TNF-α), thereby promoting PF. On the other hand, DCs suppress PF through mechanisms including the secretion of IL-10 to inhibit effector T cell activity in the lungs and promote the function of regulatory T cells (Tregs), as well as by expressing matrix metalloproteinases (MMPs) which facilitate the degradation of the extracellular matrix (ECM). This article will infer possible reasons for the different roles of DCs in PF and analyze possible reasons for the functional imbalance of DCs in pulmonary fibrosis from the complexity and changes of the pulmonary microenvironment, autophagy defects of DCs, and changes in the pulmonary physical environment.