Pulmonary fibroblasts activated by the addition of TNF-α and IL-4 enhance lymphangiogenic capacity and ameliorate lung fibrosis in an allogeneic rat model

Cytokine-stimulated pulmonary fibroblasts may serve as a novel cell source for antifibrotic therapy by modulating lymphangiogenesis and tissue remodeling, providing a potential alternative to conventional stem cell-based approaches for fibrotic lung diseases.