Transforming growth factor-beta 1 (TGF-beta 1) stimulates extracellular matrix production, and is considered a master regulator of tissue fibrosis, including idiopathic pulmonary fibrosis and radiation-induced fibrosis. A recent study identified dysregulated miR-155 expression during pulmonary fibrosis. However, the role of miR-155 in TGF-beta 1- induced pulmonary fibrosis remains unclear. In this study, we demonstrated that TGF-beta 1 downregulates miR-155 expression in human lung fibroblast cell lines. MiR-155 inhibits the pro-fibrogenic activities of TGF-beta 1 by decreasing the expression offibronectin, collagen type I, alpha 1, and alpha-smooth muscle actin. We also identified transforming growth factor-beta receptor-2 (TGFBR2) as a direct target of miR-155. Knocking down TGFBR2 in lung fibroblasts significantly decreased TGFBR2 expression and inhibited the pro-fibrogenic activities of TGF-beta 1. Expression of a miR-155- insensitive TGFBR2 construct restored fibrogenesis induced by TGF-beta 1 stimulation in miR-155 expressing cells. Therefore, our study suggests an important role for miR-155 in fibrotic lung diseases, and indicates that miR-155 is a potent therapeutic microRNA for treating pulmonary fibrosis.